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PubMed2002

The morphologic nature of noncommitted ventricular septal defects in specimens with double-outlet right ventricle.

BACKGROUND: Lev's contribution to the understanding of the morphology of hearts with double-outlet right ventricle and the surgical feasibility for correction is important and remains in current use. However, the term noncommitted ventricular septal defect remains enigmatic. The aim of this study was to elucidate the morphologic nature of the noncommitted ventricular septal defect in view of its surgical implications. METHODS: We examined 67 specimens with double-outlet right ventricle, focusing on the relationship of the ventricular septal defect to the semilunar orifices. RESULTS: The defect was subaortic, subpulmonary, or doubly committed in 55 specimens. In a further 8 specimens, the defect opened into the outlet portion of the right ventricle, but the distance between the ventricular septal defect and the semilunar orifice was extensive, either because of extreme dextroposition of the aorta or a broad ventriculoinfundibular fold, which, in some cases, was associated with a long-outlet septum. A truly noncommitted ventricular septal defect was found in the inlet in the remaining 4 specimens. An atrioventricular septal defect without extension to the outlet was present in 3 cases, and a ventricular septal defect limited to the inlet was found in another case. The ventriculoinfundibular fold, part of the outlet septum and septal band or septomarginal trabeculation, had fused to form a crestlike structure. The septomarginal trabeculation is a useful landmark in the right ventricle to differentiate the inlet from the outlet in different forms of double-outlet right ventricle. CONCLUSION: We do not suggest to discard the Lev terminology but rather to differentiate the noncommitted ventricular septal defect into 2 types: the truly noncommitted defect of the inlet type and the not-directly-committed defect, which does open into the outlet portion of the right ventricle. The implication for the surgeon is 2-fold. The tricuspid valve or right part of the atrioventricular valve is interposed between the noncommitted ventricular septal defect and the semilunar orifice. The not-directly-committed defect opens into the outlet portion of the right ventricle but is not directly subaortic or subpulmonary.

Abnormalities, Multiple↗
PubMed1999

The natural history of ventricular septal defects.

AIMS: To correlate the size and position of isolated ventricular septal defects with closure rate in a cohort of children with mean follow up of more than six years. DESIGN: A birth cohort was identified using the northern region cardiac database. The following were noted from case notes: defect size, position, means of closure, and age at closure. RESULTS: 68 children were identified. 49 defects were small, 14 were moderate, and 5 were large. 13 cases required surgical closure, including 12 perimembranous defects. 35 defects closed spontaneously. Nine of the small muscular defects remained open and five of the small perimembranous defects remained open. The spontaneous closure rate for muscular defects was significantly greater than for perimembranous defects. Mean age of follow up for patients who still have defects is 76 months. CONCLUSIONS: The position of a ventricular septal defect is extremely relevant to its natural history. Perimembranous defects accounted for most of the moderate and large defects that required surgical intervention. After more than six years almost a third of all perimembranous and just over two thirds of all muscular defects closed spontaneously.

Child, Preschool↗
PubMed1989

Colour flow imaging in the diagnosis of multiple ventricular septal defects.

Thirty one patients with multiple ventricular septal defects were studied by cross sectional echocardiography, conventional pulsed and continuous wave Doppler, colour flow imaging, and left ventriculography to determine the relative diagnostic benefits and pitfalls of each technique. The patients studied had a wide range of congenital heart defects with 19 patients having isolated multiple ventricular septal defects, three with associated tetralogy of Fallot, five with double outlet right ventricle, three with complete transposition and ventricular septal defect, and one with a complete atrioventricular septal defect. In 23 patients the defects were inspected at operation. Cross sectional imaging with integrated pulsed and continuous wave Doppler correctly identified multiple defects in only 12 (39%) patients. In contrast, colour flow imaging was accurate in 24 (77%) patients and left ventriculography in 20 (65%) patients. When patients were subdivided on the basis of relative peak systolic ventricular pressures into restrictive defects (18 patients) and non-restrictive defects (13 patients) the diagnostic value of colour flow imaging was different for each group. Colour flow mapping correctly identified multiple ventricular septal defects in 16/18 (89%) patients with restrictive defects but only 8/13 (62%) with non-restrictive defects. The comparative diagnostic accuracy of left ventriculography was 15/18 (83%) in the restrictive group and 5/13 (38%) in the non-restrictive group. Colour flow imaging was the single investigative technique with the greatest diagnostic accuracy in the diagnosis of multiple ventricular septal defects. It failed to be consistently accurate in defined subgroups with non-restrictive defects as did left ventriculography. The greatest overall diagnostic accuracy in this series was obtained when both colour flow imaging and ventriculography techniques were used in combination in a complementary fashion.

Child↗
PubMed1991

Prevalence of birth defects among low-birth-weight infants. A population study.

Major birth defects are diagnosed in about 3% to 4% of infants during their first year of life. Because many infants with birth defects have intrauterine growth retardation, are born prematurely, or both, the rate of birth defects undoubtedly varies according to the infant's birth weight. Nevertheless, the magnitude of such variation has not, to our knowledge, been adequately studied in well-defined populations. We analyzed data from the population-based Metropolitan Atlanta (Ga) Congenital Defects Program for 1978 through 1988. These data included information on 11,398 infants who were diagnosed with serious birth defects among 317,499 singleton live-born infants. Although the overall rate of birth defects was 3.6%, we observed a striking inverse relationship between the birth defects rate and the infants' birth weights. The birth defect rates were 16.2% for newborns weighing less than 1500 g at birth, 13.2% for newborns weighing from 1500 g to 1999 g, 6.2% for newborns weighing from 2000 g to 2499 g, 3.2% for newborns weighing from 2500 g to 3999 g, and 2.8% for newborns weighing 4000 g or more. Analyses by type of defect indicated that most birth defects were significantly associated with low birth weight. The higher risk of birth defects among low-birth-weight infants demonstrates that birth defects contribute to excess morbidity among low-birth-weight infants. Because of the overlap between birth defects and low birth weight, the prevention of low birth weight in the population depends greatly on a better recognition of the complex etiology of low birth weight and, in part, on the delineation of risk factors that influence the occurrence of birth defects.

Birth Rate↗
PubMed1993

Case-control study of congenital defects and parental employment in health care.

Health care workers may be occupationally exposed to known and suspected teratogens including viruses, anesthetic gases, sterilants, mercury, and x-radiation. To assess the risk of congenital defects among offspring of health care workers, we analyzed parental occupational histories for 4,915 case babies with congenital defects, registered during the years 1968-1980 by the Metropolitan Atlanta Congenital Defects Program (MACDP) registry, and for 3,027 control babies born without defects during the same period. Offspring of mothers employed in a nursing occupation during the periconceptional period had a modest excess risk of having at least one congenital defect (relative risk [RR] = 1.42; 95% confidence interval [CI] 1.06-1.88); the offspring were at statistically significant increased risk of having anencephaly or spina bifida (RR = 2.00; 95% CI 1.01-4.30), coarctation of the aorta (RR = 2.06; 95% CI 1.10-3.82), genital system defects (RR = 1.61; 95% CI 1.03-2.53), and urinary system defects (RR = 3.43; 95% CI 1.41-8.34). These associations were not confounded by maternal age, education, or alcohol consumption. Offspring of mothers employed in administrative or clerical jobs in the health care industry also had a modest excess risk of defects (RR = 1.35; 95% CI 0.96-1.90), including a statistically significant excess risk of limb defects. We also found associations between neural tube defects and potential exposure to anesthetic gases and to x-radiation, but each association was based on only three case babies of potentially exposed parents. We found no associations between defects and paternal health care employment, except for a few individual defects, and these were based on small numbers of exposed subjects. Only one of five previous studies reviewed found an increased risk of congenital defects among offspring of nurses, but three of the four negative studies had substantially smaller sample sizes than the present study. Detection bias may be a possible explanation for the apparent excess risk of certain defects among offspring of nurses.

Abnormalities, Drug-Induced↗
PubMed1990

On the measurement and interpretation of birth defect associations in epidemiologic studies.

The extent of clustering of 2 or more defects in the same infant can be expressed as the ratio of the observed number of infants with the defects (O) over the expected number of such infants (E). The expected is usually derived from the product of population rates of individual defects. Because large O/E ratios are obtained for many defect combinations, it has been suggested that clustering of defects is generalized and nonspecific. To control for the tendency of nonspecific clustering of defects, an alternative method is to perform the same calculations among multimalformed infants only. A main limitation of this method is that it adjusts for the clustering tendency of all defects rather than the ones of interest, often resulting in spuriously low O/E ratios. We present a new method to adjust for the tendency for nonspecific clustering between defects that overcomes this limitation. With this method, adjusted O/E ratios are inversely related to the proportion of infants who are multimalformed and have one or more of the defects being examined. Using data from the Metropolitan Atlanta Congenital Defects Program, we apply this method to the previously described associations among VACTERL defects and midline or "schisis" defects. We show that adjusted O/E ratios obtained are greater than those obtained by using multimalformed infants. For midline defects, many of the adjusted ratios were close to one, indicating nonspecific clustering of these defects. Finally, using the example of isotretinoin embryopathy, we show that O/E ratios depend highly on the frequency of exposure in the population, and thus, they should be interpreted with caution.

Abnormalities, Drug-Induced↗
PubMed1994

Congenital abnormalities associated with limb deficiency defects: a population study based on cases from the Hungarian Congenital Malformation Registry (1975-1984).

Limb deficiency defects (LD) occurring among 1,575,904 births in Hungary during 1975-1984 were reviewed. The overall birth prevalence of LD was 1 in 1,816. This paper discusses the nature and distribution of the limb and other defects in the 275 (32%) children who had structural malformations in other systems. Two main forms of classification were used: morphologic and causal. Additional malformations were most commonly seen in infants with amelia, rudimentary limb (RL), radial/tibial (RT), intercalary or central axis (CA) LD and rarely in those with terminal transverse (TT) or ulnar/fibular (UF) defects. Upper limbs (81%) were involved significantly more often than lower limbs (42%) and there were more right-sided defects (83% vs. 71%) due to an excess of right arm involvement especially with radial ray and split hand anomalies. Single limb involvement was relatively common with amelia (88%), UF (82%), RT (50%), and TT (50%) defects. With other LD, multimelic involvement was more characteristic. This was usually symmetric with intercalary and RL defects but asymmetric with CA anomalies and digital deficiencies (DD). From a causal perspective, 17% of cases had genetic disorders, 52% had recognized associations, anomalies, sequences, environmental causes or patterns of unknown origin, and 31% had unknown patterns of malformations. The commonest entities were amnion disruption sequence (16% of cases) and VACTERL association (8%). Both of these disorders showed unusual temporal distribution. As anticipated, patterns of malformations differed with the type of LD. Amelia and digital amputations were often seen with body wall defects, atypical anencephaly or encephalocele, and cleft lip reflecting amnion disruption. Rudimentary limb was seen with anencephaly, omphalocele, renal agenesis, aberrant genitalia, and imperforate anus, reflecting defects of blastogenesis including the cloacal exstrophy and caudal regression sequences and Schisis association. Radial/tibial defects were associated with different patterns depending on whether the limb defects were unilateral or bilateral. Unilateral defects occurred with anomalies suggesting VACTERL association or the facio-auriculo-vertebral anomaly, while bilateral defects occurred more often in genetic or potentially genetic disorders including VACTERL with hydrocephalus. Central axis defects showed three main patterns of association: one reflecting the ectrodactyly-ectodermal dysplasia-clefting syndrome; one with tongue anomalies representing a variant of oro-mandibular-limb (Hanhart) anomaly, and the last with hydronephrosis indicating a group of "acro-renal" syndromes. Strong associations with other anomalies were not seen in the groups with TT, UF, or intercalary defects.

Abnormalities, Multiple↗
PubMed2003

First-year mortality rates for selected birth defects, Hawaii, 1986-1999.

Birth defects have been the leading cause of infant death in the United States for over the last decade. However, there is little population-based data on the first-year mortality rates for many specific birth defects and the factors that may affect these mortality rates. This investigation examined the first-year mortality rates for 54 selected birth defects of various organ systems in Hawaii during 1986-1999 using data from a population-based birth defects registry and evaluated the impact of the presence of chromosomal abnormalities and other structural birth defects and the year of delivery on the mortality rates. Mortality rates varied widely by defect, being highest for anencephaly (100%), trisomy 13 (82%), and trisomy 18 (74%), while no first-year deaths were reported for glaucoma, bladder exstrophy, and persistent cloaca. The majority (36 of 54 or 67%) of the birth defects had a mortality rate of less than 25%. Among the 51 structural birth defects, 38 (75%) had higher first-year mortality rate for cases with chromosomal abnormalities and 42 (82%) had higher first-year mortality rates for cases with other major structural birth defects. The mortality rate among 1986-1992 deliveries was higher than the mortality rate among 1993-1999 deliveries for 37 (69%) of the 54 birth defects. This study indicates that first-year mortality rates vary widely by type of birth defect, although the mortality rate for the majority of birth defects is relatively low. The presence of a chromosomal abnormality or other structural birth defect increases the mortality rate, and mortality rates for the majority of birth defects have declined in Hawaii during the study period.

Congenital Abnormalities↗
PubMed2004

Impact of excluding cases with known chromosomal abnormalities on the prevalence of structural birth defects, Hawaii, 1986-1999.

Chromosomal abnormalities are more common in the presence of structural birth defects. However, much of the literature have only provided chromosomal abnormality rates for one or a few structural birth defects at a time. This study calculated the chromosomal abnormality rates for a number of structural birth defects using data from the Hawaii Birth Defects Program (HBDP) for deliveries during 1986-1999 and evaluated the impact of exclusion of cases with chromosomal abnormalities when calculating birth prevalence. The chromosomal abnormality rates were highest for endocardial cushion defect (40%) and omphalocele (27%), while no chromosomal abnormalities were reported for pyloric stenosis, persistent cloaca, and deficiency of lower limbs. The majority of chromosomal abnormality rates fell within a certain range, with 32 (63%) of the birth defect categories having chromosomal abnormality rates of 5-15%. The chromosomal abnormality rates also tended to be higher for multiple than for isolated cases. For three of the structural birth defects (ventricular septal defect, atrial septal defect, endocardial cushion defect), the birth prevalence of the defect, when cases with a chromosomal abnormality were excluded, was significantly lower than the birth prevalence that included those cases. Chromosomal abnormality rates varied by type of structural birth defect and presence of other major structural birth defects. For at least several structural birth defects, exclusion of cases with chromosomal abnormalities significantly underestimated the birth prevalence. This underestimation may be important, depending on the purpose of the analysis.

Chromosome Aberrations↗
PubMed1997

Defects of the respiratory chain in the normal human liver and in cirrhosis during aging.

Defects of the respiratory chain are a typical feature of mitochondrial diseases and occur also during normal aging where they have been described in postmitotic tissues. The present study addresses the question of defect expression in the normal and cirrhotic liver. Randomly distributed defects of complex III (ubiquinone-cytochrome-c-oxidoreductase) and of complex IV (cytochrome-c-oxidase) of the respiratory chain have been detected with age-related increasing frequency both in normal and cirrhotic livers. No defects were present for complex II (succinate-dehydrogenase) and complex V (adenosine triphosphate-synthase) and in liver cell carcinomas. Sixty-one of 107 normal livers (57%) showed defects of the respiratory chain. The defects occurred in advanced age (over 50 years) in 87%. In contrast 50 of 64 cirrhotic livers (78%) had defects and approximately 60% occurred after age 50. The defects were caused by a loss of enzyme protein involving both nuclearly and mitochondrially coded subunits. Ninety-four percent of the defects (n = 275) involved complex IV selectively. In 4% selective defects of complex III were found and combined defects of both complexes occurred in only 2%. In situ hybridization and polymerase chain reaction (PCR) studies for the detection of the common deletion (4.977 bp) and of various point mutations of mitochondrial DNA (mtDNA) revealed no consistent molecular genetic abnormalities in microdissected respiratory chain defective liver cell areas. Single point mutations at nt 3243 and/or 5692 were found only in 7 of 18 microdissected probes from 6 patients. The results show that defects of the respiratory chain occur already in normal livers most probably during cell aging and at a higher rate in cirrhosis. The random defect pattern favors a stochastic process, e.g., free radical damage. However, the role of mutations of mtDNA remains to be established.

Adenosine Triphosphatases↗
PubMed2005

Changing incidence, type, and natural history of conduction defects after coronary artery bypass grafting.

BACKGROUND: Cardiac conduction defects occur after cardiac surgery. We hypothesized that population aging and increased use of beta-blockers would increase the incidence of new conduction defects after coronary surgery. METHODS: We examined the medical records of 800 coronary artery bypass grafting (CABG) patients (400 from 1991 and 400 from 2001). Exclusion criteria included the following: preexisting conduction defect, permanent pacemaker, and perioperative atrial fibrillation, leaving 303 and 269 patients, respectively, included in the two study years. The incidence, type, and persistence of new conduction defects were determined from the preoperative, postoperative, and the predischarge electrocardiogram. Multivariate analysis identified predictors of new defects. RESULTS: Study populations were well-matched. There was a marked decrease in the incidence of new postoperative conduction defects from 1991 (19%) to 2001 (6%). There was also a change in the most frequently occurring block, from a right-bundle-branch-block in 1991 (10%) to first-degree atrioventricular block (3%) in 2001. Finally, conduction defects in 1991 were more transient. While 19% of 1991 patients showed a conduction defect early postoperatively, only 9% were persistent. In 2001, the incidence of conduction defects at discharge (7%), was equivalent to that early postoperatively (6%). Predictors of new conduction defects included year of operation, age, intraaortic balloon counterpulsation, number of vessels bypassed, and crystalloid cardioplegia. CONCLUSIONS: Our results were the opposite of those predicted. Our report identifies a changing incidence, type, and natural history of conduction defects after CABG. Our comparison demonstrated a decrease in the incidence of new conduction defects, as well as a qualitative change in the defects identified. Multivariate analysis provided predictors of new conduction defects after CABG.

Adult↗
PubMed2000

The open section effect in a long bone with a longitudinal defect - a theoretical modeling study.

A longitudinal defect dramatically alters the stress distribution within a long bone. The altered stress distribution can influence the structural properties of the bone and the stimulus for repair and remodeling of the defect and the surrounding bone. For applied torsion, the defect interrupts the normal shear flow around the bone. Reversal of the shear flow along the inner cortex of the bone is the primary characteristic of the "open-section" effect. Stress concentration effects also produce large stresses at the defect corners. A finite element model of a femur mid-diaphysis with a rectangular defect in the posterior cortex was developed to quantify the femur stress distribution and torsional stiffness for defect widths ranging from one-tenth of the femur outer diameter (0.1 OD) to 0.3 OD, and defect lengths ranging from 0.5 to 5 OD. Defects with a length of 1 OD or shorter had little influence on the femur torsional stiffness or the femur shear-stress distribution. The torsional stiffness decreased most dramatically as the defect length increased from 2 to 3 OD, but began to approach an asymptote near 5 OD. Shear flow reversal peaked at the center of the defect for defects longer than 1 OD, and the magnitude of the reversal began to approach an asymptote near 5 OD. For each defect, the largest stresses within the bone, developed at the defect corners. The results indicate that the open-section effect decreases the torsional stiffness and stress concentration effects decrease the torsional strength of a long bone with a longitudinal defect.

Biomechanical Phenomena↗
PubMed1998

Chondrocyte-seeded collagen matrices implanted in a chondral defect in a canine model.

The objective of our study was to evaluate reparative tissues formed in chondral defects in an adult canine model implanted with cultured autologous articular chondrocytes seeded in type I and II collagen GAG matrices. Two defects were produced in the trochlea grooves of the knees of 21 dogs, with cartilage removed down to the tidemark. This study includes the evaluation of 36 defects distributed among five treatment groups: Group A, type II collagen matrix seeded with autologous chondrocytes under a sutured type II collagen flap; Group B, type I collagen matrices seeded with chondrocytes under a sutured fascia flap; Group C, unseeded type I collagen matrix implanted under a sutured fascia flap; Group D, fascia lata flap alone; and Group E, untreated defects. All animals were killed 15 weeks after implantation. Six other defects were created at the time of death and evaluated immediately after production as 'acute defect controls'. In three additional defects, unseeded matrices were sutured to the defect and the knee closed and reopened after 30 min to determine if early displacement of the graft was occurring; these defects served as 'acute implant controls'. The areal percentages of four tissue types in the chondral zone of the original defect were determined histomorphometrically: fibrous tissue (FT); hyaline cartilage (HC); transitional tissue (TT, including fibrocartilage); and articular cartilage (AC). New tissue formed in the remodeling subchondral bone underlying certain defects was also assessed. Bonding of the repair tissue to the subchondral plate and adjacent cartilage, and degradation of the adjacent tissues were evaluated. There were no significant differences in the tissues filling the original defect area of the sites treated with chondrocyte-seeded type I and type II matrices. Most of the tissue in the area of the original defect in all of the groups was FT and TT. The areal percentage of HC plus AC was highest in group E, with little such tissue in the cell-seeded groups, and none in groups C and D. The greatest total amount of reparative tissue, however, was found in the cell-seeded type II matrix group. Moreover, examination of the reparative tissue formed in the subchondral region of defects treated with the chondrocyte-seeded collagen matrices (Groups A and B) demonstrated that the majority of the tissue was positive for type II collagen and stained with safranin O. These results indicate an influence of the exogenous chondrocytes on the process of chondrogenesis in this site. In all groups with implants (A-D), 30(50% of the FT and TT was bonded to the adjacent cartilage. Little of this tissue (6-22%) was attached to the subchondral plate, which was only about 50% intact. Remarkable suture damage was found in sections from each group in which sutures were used. Harvest sites showed no regeneration of normal articular cartilage, 18 weeks after the biopsy procedure. Future studies need to investigate other matrix characteristics, and the effects of cell density and incubation of the seeded sponges prior to implantation on the regenerative response.

Animals↗
PubMedDate not supplied

Metalloproteinases (MMPs -2, -3) are involved in TGF-beta and IGF-1-induced bone defect healing in 20-month-old female rats.

Matrix metalloproteinases are important in the physiological and pathological degradation of extracellular matrix including that of bone and cartilage. The process of bone defect healing is associated with formation of cartilage callus and cancelous bone. With maturation and aging, the response of skeletal tissues to injury is limited. The ability of growth factors to enhance bone defect healing in aged rats was studied. Partial bone defects were induced in femurs of aged rats. A single dose of IGF-1, TGF-beta+IGF-1 or saline was inserted in the defect and bones were examined after 2 and 4 weeks. Morphology revealed that after 2 weeks of treatment with TGF-beta the defects were filled with mesenchyme-like tissue and delicate bone trabeculae. Positive staining for metalloproteinase-2 (MMP-2) was shown at the sites of new bone formation. In defects treated with IGF-1 or TGF-beta+IGF-1 nodules of cartilage and fine bone trabeculae along with positive staining for both MMP-2 and MMP-3 were demonstrated in the healing defects. After 4 weeks radiology revealed mineralization in defects treated with TGF-beta and less pronounced mineralization after treatment with IGF-1, or with TGF-beta+IGF-1, whereas only partial healing of the defects was observed in control specimens. MMP-2 and MMP-3 were detected at sites of new bone formation after treatment with TGF-beta, IGF-1, and TGF-beta+IGF-1. It is concluded that TGF-beta and IGF-1 induced bone defect healing in aged rats. TGF-beta induced bone formation while IGF-1 induced cartilage and than bone formation via endochondral ossification. The localization of MMP-2 and MMP-3 in the healing defects reflected the synthesis of bone or cartilage matrices in the defect, reflecting the involvement of MMPs in the process of bone formation and endochondral ossification. The ability to induce bone defect healing in aging is of great clinical importance and understanding the involvement of MMPs in this process can contribute to future treatment with growth factors to enhance bone defect healing in 20-month-old female rats.

Journal Article↗
PubMedDate not supplied

Quantitative comparison of single-isotope and dual-isotope stress-rest single-photon emission computed tomographic imaging for reversibility of defects.

BACKGROUND: Dual-isotope rest/stress single-photon emission computed tomographic (SPECT) imaging is a time-saving imaging protocol. However, the stress radiotracer, technetium 99m-labeled sestamibi, and the rest radiotracer, thallium 201, have different physical properties and myocardial kinetics. In patients with abnormal resting myocardial perfusion, these differences may affect quantification of rest defect size and defect reversibility. The purpose of the study was to compare myocardial perfusion defect reversibility quantitatively by single-isotope (rest/stress sestamibi) and dual-isotope (rest thallium/stress sestamibi) SPECT. METHODS AND RESULTS: Thirty patients with prior myocardial infarction underwent rest/stress sestamibi SPECT imaging and rest thallium SPECT imaging. Defects were quantified according to circumferential count profiles with a normal sestamibi database. The images of a subgroup of 21 patients were processed with radiotracer-specific normal databases. Defect size and defect reversibility were compared quantitatively for single-isotope and dual-isotope SPECT. Rest sestamibi defect size was significantly larger than rest thallium defect size (19 +/- 15 vs 14 +/- 16; p = 0.007). Defect reversibility was larger with thallium than with sestamibi (10 +/- 9 vs 6 +/- 6; p = 0.002). With radiotracer-specific normal databases, mean rest sestamibi and thallium defect sizes in 21 patients were not different (23 +/- 19 vs 21 +/- 17; difference not significant). With radiotracer-specific normal databases, mean defect reversibility was not different with either sestamibi or thallium (6 +/- 6 vs 8 +/- 9; difference not significant), although correlation among individual patients was only fair (r2 = 0.48). CONCLUSION: In patients with prior myocardial infarction, stress-induced defect reversibility is quantitatively larger with dual-isotope imaging than with single-isotope imaging. Quantitative processing of dual-isotope images requires radiotracer-specific normal databases. Because of different characteristics of sestamibi and thallium, assessment of defect reversibility on dual-isotope images should be made with caution. Only relatively large defect reversibility can be assumed to represent true stress-induced myocardial ischemia.

Dipyridamole↗
PubMed1998

Bioactive glass granules and polytetrafluoroethylene membrane in the repair of bone defects adjacent to titanium and bioactive glass implants.

An experimental animal model was used to investigate the effect of bioactive glass (BG) granules and nonresorbable polytetrafluoroethylene (PTFE) membrane on the repair of cortical bone defects adjacent to titanium and BG implants. Thirty-two Astra(R) (diameter 3.5 mm) dental implants were inserted bicortically and 42 conical BG implants (diameter 2.5-3.0 mm) monocortically, into fitted holes of rabbit tibia. Before implantation, a standardized bone defect was created by drilling an extra hole (diameter 3.0 mm) adjacent to each implant site. Twenty-eight defects were filled with BG granules (diameter 630-800 microm) (BG group) and 28 defects were left empty but covered with PTFE membrane (PTFE group). No material was used in 18 control defects (control group). Morphometrical evaluation with a digital image analysis system was used to measure bone repair as percentages of the defect area on scanning electron microscopy (SEM) and light microscopy pictures. Bone-implant contact was measured as percentages of the thickness of the cortical bone. At 6 and 12 wk, bone repair in defects in connection with titanium implants was 23.2% and 36.6% in the BG group, 23.2% and 32.4% in the PTFE group, and 47.2% and 46.2% in control defects. Corresponding figures for BG implants were 33.2% and 40.1% in the BG group, 16.6% and 33.5% in the PTFE group, and 25.7% and 54.9% in control defects, BG granules and new bone together filled 82.7% and 68.5% of the defect area adjacent to titanium implants, and 75.9% and 74.4% of the defect adjacent to BG implants at 6 and 12 wk, respectively. Better bone-implant contact was achieved at the defect side with BG than titanium implants (77.0% versus 45.0% at 12 wk). The results indicate that BG granules are useful in treatment of bone defects adjacent to dental implants. BG coating of the implant seems to improve osseointegration in the defect area.

Journal Article↗
PubMedDate not supplied

Arthroscopic subchondral bone plate microfracture technique augments healing of large chondral defects in the radial carpal bone and medial femoral condyle of horses.

OBJECTIVE: To evaluate the effect of arthroscopic subchondral bone microfracture on healing of large chondral defects in horses. STUDY DESIGN: Short- (4 months) and long-term (12 months) in vivo experimental chondral defect model. ANIMALS: 10 horses, aged 2 to 5 years. METHODS: Each horse had a 1 cm2 full-thickness chondral defect created in both radial carpal bones and both medial femoral condyles. One carpus and one femoral condyle of each horse had the subchondral bone plate under the defect perforated using an orthopedic awl. All horses were exercised, five horses were evaluated after 4 months and five horses after 12 months. Gross, histologic, and histomorphometric examination of defect sites and repair tissues was performed, as was collagen typing of the repair tissue. RESULTS: On gross observation a greater volume of repair tissue filled treated defects (74%) compared with control defects (45%). Histomorphometry confirmed more repair tissue filling treated defects, but no difference in the relative amounts of different tissue types was observed. There was an increased percentage of type II collagen in treated defects compared with control defects and evidence of earlier bone remodeling as documented by changes in porosity. CONCLUSIONS: In full-thickness chondral defects in exercised horses, treatment with subchondral bone microfracture increased the tissue volume in the defects and the percentage of type II collagen in the tissue filling the defects when compared to nontreated defects. CLINICAL RELEVANCE: No negative effects of the microfracture technique were observed and some of the beneficial effects are the basis for recommending its use in patients cases with exposed subchondral bone.

Animals↗
PubMed1994

A population-based study of the risk of recurrence of birth defects.

BACKGROUND: Certain birth defects are known to recur in families, but most estimates of the risk of recurrence have come from clinic-based studies. In this study we estimated the risk of recurrent birth defects using a population-based registry. METHODS: The study was based on the records of the first and second infants delivered by 371,933 women from 1967 through 1989. The records are maintained by the Medical Birth Registry of Norway. For the 9192 women whose first infant had a birth defect, we determined the relative risk of similar and dissimilar defects in the second infant. The reference population was women whose first infant had no defect. RESULTS: Among first infants, 2.5 percent had a birth defect. The mothers of affected first infants were 2.4 times as likely as other women to have second infants with any registered defect. This increased risk was due primarily to an increased (7.6 times higher) risk of the same defect in the second infant as in the first (95 percent confidence interval, 6.5 to 8.8) and secondarily to a slightly increased (1.5 times higher) risk of a different defect in the second infant (95 percent confidence interval, 1.3 to 1.7). Among the women who lived in the same municipality during both pregnancies, the relative risk of having a second infant with the same defect was 11.6, as compared with 5.1 among the women who moved to another municipality after the birth of their first infant (P < 0.001). CONCLUSIONS: Among women whose first infant has a birth defect, the risk of the same defect in the second infant is substantially increased and the risk of a different defect in the second infant is slightly increased. Environment plays a strong part in repeated defects.

Confidence Intervals↗