Both initial red cell distribution width (RDW) and change in RDW during heart failure hospitalization are associated with length of hospital stay and 30-day outcomes.

INTRODUCTION: We examined the predictive ability of red cell distribution width (RDW) and the change in RDW during hospitalization (ΔRDW) for length of stay (LOS) and 30-day outcomes after heart failure (HF) inpatient stay. METHODS: Electronic query of Intermountain Healthcare medical records identified patients (N = 6414) with a primary diagnosis of HF who were discharged between 2004 and 2013, had RDW measured within 24 h after admission, and had RDW tested at least once more during the same hospitalization. ΔRDW was defined as the last RDW within 24 h prior to discharge minus the first RDW. RESULTS: Median LOS by initial RDW quartiles was Q1: 3.0, Q2: 3.1, Q3: 3.7, and Q4: 4.0 days (P-trend<0.001), and by ΔRDW quartiles was Q1: 4.1, Q2: 3.4, Q3: 3.6, and Q4: 4.7 days (P-trend<0.001). Both initial RDW (16.8 ± 2.8% vs. 16.3 ± 2.7%, P < 0.001) and ΔRDW (0.21 ± 1.09% vs. 0.14 ± 1.04%, P = 0.039) predicted 30-day readmission vs. no readmit. For 30-day decedents vs. survivors, initial RDW was 17.3 ± 3.0% vs. 16.3 ± 2.6% (P < 0.001), while ΔRDW was +0.20 ± 1.14% vs. +0.14 ± 1.04% (P = 0.15). CONCLUSIONS: Greater initial RDW and ΔRDW during HF hospitalization were associated with 30-day mortality, longer LOS, and 30-day all-cause readmission, suggesting both ΔRDW and initial RDW may aid in personalizing prognosis and treatment.

Generating genetic risk scores from intermediate phenotypes for use in association studies of clinically significant endpoints.

While previous results of genetic association studies for common, complex diseases (eg., coronary artery disease, CAD) have been disappointing, examination of multiple related genes within a physiologic pathway may provide improved resolution. This paper describes a method of calculating a genetic risk score (GRS) for a clinical endpoint by integrating data from many candidate genes and multiple intermediate phenotypes (IPs). First, the association of all single nucleotide polymorphisms (SNPs) to an IP is determined and regression beta-coefficients are used to calculate an IP-specific GRS for each individual, repeating this analysis for every IP. Next, the IPs are assessed by a second regression as predictors of the clinical endpoint. Each IP's individual GRS is then weighted by the regression beta-coefficients from the second step, creating a single, composite GRS. As an example, 3,172 patients undergoing coronary angiography were evaluated for 3 SNPs from the cholesterol metabolism pathway. Although these data provide only a preliminary example, the GRS method detected significant differences in CAD by GRS group, whereas separate genotypes did not. These results illustrate the potential of the GRS methodology for multigenic risk evaluation and suggest that such approaches deserve further examination in common, complex diseases such as CAD.

Femoral arterial puncture management after percutaneous coronary procedures: a comparison of clinical outcomes and patient satisfaction between manual compression and two different vascular closure devices.

BACKGROUND: Vascular access site management is crucial to safe, efficient and comfortable diagnostic or interventional transfemoral percutaneous coronary procedures. Two new femoral access site closure devices, Perclose and Angio-Seal , have been proposed as alternative methods to manual compression (MC). We compared these two devices and tested them in reference to standard MC for safety, effectiveness and patient preference. METHODS: Prospective demographic, peri-procedural, and late follow-up data for 1,500 patients undergoing percutaneous coronary procedures were collected from patients receiving femoral artery closure by MC (n = 469), Perclose (n = 492), or Angio-Seal (n = 539). Peri-procedural, post-procedural, and post-hospitalization endpoints were: 1) safety of closure method; 2) efficacy of closure method; and 3) patient satisfaction. RESULTS: Patients treated with Angio-Seal experienced shorter times to hemostasis (p < 0.0001, diagnostic and interventional) and ambulation (diagnostic, p = 0.05; interventional, p < 0.0001) than those treated with Perclose. Those treated with Perclose experienced greater access site complications (Perclose vs. Angio-Seal, p = 0.008; Perclose vs. MC, p = 0.06). Patients treated with Angio-Seal reported greater overall satisfaction, better wound healing and lower discomfort (each vs. Perclose or vs. MC, all p < or = 0.0001). For diagnostic cath only, median post-procedural length of stay was reduced by Angio-Seal (Angio-Seal vs. MC, p < 0.0001; Angio-Seal vs. Perclose, p = 0.009). No difference was seen in length of stay for interventional cases. CONCLUSIONS: Overall, Angio-Seal performed better than Perclose or MC in reducing time to ambulation and length of stay among patients undergoing diagnostic procedures. There was a higher rate of successful deployment and shorter time to hemostasis for Angio-Seal, and this was accomplished with no increase in bleeding complications throughout the follow-up. Additionally, Angio-Seal performed better than Perclose in exhibiting a superior 30-day patient satisfaction and patient assessment of wound healing with less discomfort.

Usefulness of in-hospital prescription of statin agents after angiographic diagnosis of coronary artery disease in improving continued compliance and reduced mortality.

Despite well-documented clinical benefit of the use of statins in patients with coronary artery disease (CAD) and even mild lipid elevations, studies have documented the presence of a significant "treatment gap" between those patients in whom treatment is indicated and those patients who actually receive it. It has been proposed that a prescription for statin therapy given to indicated patients at the time of initial angiographic diagnosis of CAD has the potential to improve long-term medication compliance, but this requires further evaluation. We prospectively followed 600 patients with angiographically demonstrated CAD (diameter stenosis > or = 70%) who met the National Cholesterol Education Project (NCEP) guidelines for statin therapy for an average of 3.0 years (range 2.0 to 4.6). Patients were an average of 65 years of age, 78% were men, 77% presented initially with acute ischemic syndrome, and 64 (10.7%) died during follow-up. Overall, 105 patients (18%) were discharged from the initial hospitalization with a statin prescription. At long-term follow-up, the number of patients taking statins had increased to 47%. However, long-term statin compliance was significantly higher among patients initially discharged with a statin prescription than those who were not (77% vs 40%; p < 0.0001). Additionally, those patients discharged with a statin prescription had significantly reduced mortality rate at long-term follow-up (5.7% vs 11.7%; p = 0.05). Cox hazard regression analysis, controlling for all known clinical baseline variables, confirmed the absence of a prehospital discharge statin prescription to be an independent predictor of increased mortality (hazard ratio 2.4) with a statistical trend (p = 0.06). Thus, this study demonstrates that after angiographic diagnosis of CAD, prescription of appropriate statin therapy at the time of hospital discharge improves long-term statin compliance and may significantly enhance survival.

Statin therapy, lipid levels, C-reactive protein and the survival of patients with angiographically severe coronary artery disease.

OBJECTIVES: The joint predictive value of lipid and C-reactive protein (CRP) levels, as well as a possible interaction between statin therapy and CRP, were evaluated for survival after angiographic diagnosis of coronary artery disease (CAD). BACKGROUND: Hyperlipidemia increases risk of CAD and myocardial infarction. For first myocardial infarction, the combination of lipid and CRP levels may be prognostically more powerful. Although lipid levels are often measured at angiography to guide therapy, their prognostic value is unclear. METHODS: Blood samples were collected from a prospective cohort of 985 patients diagnosed angiographically with severe CAD (stenosis > or =70%) and tested for total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and CRP levels. Key risk factors, including initiation of statin therapy, were recorded, and subjects were followed for an average of 3.0 years (range: 1.8 to 4.3 years) to assess survival. RESULTS: Mortality was confirmed for 109 subjects (11%). In multiple variable Cox regression, levels of TC, LDL, HDL and the TC:HDL ratio did not predict survival, but statin therapy was protective (adjusted hazard ratio [HR] = 0.49, p = 0.04). C-reactive protein levels, age, left ventricular ejection fraction and diabetes were also independently predictive. Statins primarily benefited subjects with elevated CRP by eliminating the increased mortality across increasing CRP tertiles (statins: HR = 0.97 per tertile, p-trend = 0.94; no statins: HR = 1.8 per tertile, p-trend < 0.0001). CONCLUSIONS: Lipid levels drawn at angiography were not predictive of survival in this population, but initiation of statin therapy was associated with improved survival regardless of the lipid levels. The benefit of statin therapy occurred primarily in patients with elevated CRP.

Cytomegalovirus seropositivity and C-reactive protein have independent and combined predictive value for mortality in patients with angiographically demonstrated coronary artery disease.

BACKGROUND: The role of inflammation in coronary artery disease (CAD) is being increasingly recognized. Markers of inflammation (eg, C-reactive protein [CRP]) and infection (eg, seropositivity to Chlamydia pneumoniae, cytomegalovirus [CMV], and Helicobacter pylori) have been proposed as risk factors for CAD, but these associations require further evaluation. METHODS AND RESULTS: We prospectively tested whether CRP levels and IgG seropositivity to C pneumoniae, CMV, and H pylori are predictors of subsequent mortality in 985 consecutive patients with angiographically demonstrated CAD (stenosis >/=70%). Patients were followed for an average of 2.7 years (range 1.5 to 4.0 years). Patients averaged 65 years of age; 77% were men; and 110 (11.2%) died during follow-up. CRP levels were significantly elevated in nonsurvivors compared with survivors (mean CRP 3.1 mg/dL versus 1.5 mg/dL, P:=0.003). After controlling for all known baseline variables, the 2nd and 3rd tertiles of CRP compared with the 1st produced a Cox hazard ratio (HR) for mortality of 2.4 (P:=0.001). Of the 3 infectious markers tested, only seropositivity to CMV (HR=1.9, P:<0.05) was predictive of mortality. The majority of mortality risk associated with elevated CRP or CMV seropositivity occurred when both risk factors were present (P: for trend <0.0001). Other independent predictors of increased risk of mortality were age (HR=1.07 per year, P:<0.0001), left ventricular ejection fraction (HR=0.97 per percent, P:<0.0001), and diabetes mellitus (HR=1.7, P:=0.02). CONCLUSIONS: CMV seropositivity and elevated CRP, especially when in combination, are strong, independent predictors of mortality in patients with CAD. This suggests an interesting hypothesis that a chronic, smoldering infection (CMV) might have the capacity to accelerate the atherothrombotic process.

A common variant of the AMPD1 gene predicts improved cardiovascular survival in patients with coronary artery disease.

OBJECTIVE: We tested whether a common AMPD1 gene variant is associated with improved cardiovascular (CV) survival in patients with coronary artery disease (CAD). BACKGROUND: Reduced activity of adenosine monophosphate deaminase (AMPD) may increase production of adenosine, a cardioprotective agent. A common, nonsense, point variant of the AMPD1 gene (C34T) results in enzymatic inactivity and has been associated with prolonged survival in heart failure. METHODS: Blood was collected from 367 patients undergoing coronary angiography. Genotyping was done by polymerase chain reaction amplification and restriction enzyme digestion, resulting in allele-specific fragments. Coronary artery disease was defined as > or =70% stenosis of > or =1 coronary artery. Patients were followed prospectively for up to 4.8 years. Survival statistics compared hetero- (+/-) or homozygotic (-/-) carriers with noncarriers. RESULTS: Patients were 66 +/- 10 years old; 79% were men; 22.6% were heterozygous and 1.9% homozygous for the variant AMPD1(-) allele. During a mean of 3.5 +/- 1.0 years, 52 patients (14.2%) died, 37 (10.1%) of CV causes. Cardiovascular mortality was 4.4% (4/90) in AMPD1(-) allele carriers compared with 11.9% (33/277) in noncarriers (p = 0.046). In multiple variable regression analysis, only age (hazard ratio, 1.11/year, p < 0.001) and AMPD1(-) carriage (hazard ratio, 0.36, p = 0.053) were independent predictors of CV mortality. CONCLUSIONS: Carriage of a common variant of the AMPD1 gene was associated with improved CV survival in patients with angiographically documented CAD. The dysfunctional AMPD1(-) allele may lead to increased cardiac adenosine and increased cardioprotection during ischemic events. Adenosine monophosphate deaminase-1 genotyping should be further explored in CAD for prognostic, mechanistic and therapeutic insights.

Plasma homocysteine predicts mortality independently of traditional risk factors and C-reactive protein in patients with angiographically defined coronary artery disease.

BACKGROUND: Plasma homocysteine (tHCY) has been associated with coronary artery disease (CAD). We tested whether tHCY also increases secondary risk, after initial CAD diagnosis, and whether it is independent of traditional risk factors, C-reactive protein (CRP), and methylenetetrahydrofolate reductase (MTHFR) genotype. METHODS AND RESULTS: Blood samples were collected from 1412 patients with severe angiographically defined CAD (stenosis >/=70%). Plasma tHCY was measured by fluorescence polarization immunoassay. The study cohort was evaluated for survival after a mean of 3.0+/-1.0 years of follow-up (minimum 1.5 years, maximum 5.0 years). The average age of the patients was 65+/-11 years, 77% were males, and 166 died during follow-up. Mortality was greater in patients with tHCY in tertile 3 than in tertiles 1 and 2 (mortality 15.7% versus 9.6%, P:=0.001 [log-rank test], hazard ratio [HR] 1.63). The relative hazard increased 16% for each 5-micromol/L increase in tHCY (P:<0.001). In multivariate Cox regression analysis, controlling for univariate clinical and laboratory predictors, elevated tHCY remained predictive of mortality (HR 1.64, P:=0.009), together with age (HR 1. 72 per 10-year increment, P:<0.0001), ejection fraction (HR 0.84 per 10% increment, P:=0.0001), diabetes (HR 1.98, P:=0.001), CRP (HR 1. 42 per tertile, P:=0.004), and hyperlipidemia. Homozygosity for the MTHFR variant was weakly predictive of tHCY levels but not mortality. CONCLUSIONS: In patients with angiographically defined CAD, tHCY is a significant predictor of mortality, independent of traditional risk factors, CRP, and MTHFR genotype. These findings increase interest in tHCY as a secondary risk marker and in secondary prevention trials (ie, with folate/B vitamins) to determine whether reduction in tHCY will reduce risk.

Lack of association of a common polymorphism of the plasminogen activator inhibitor-1 gene with coronary artery disease and myocardial infarction.

OBJECTIVES: The study was done to assess whether the common polymorphic allele (4G) of the plasminogen activator inhibitor-1 (PAI-1) gene is associated with coronary artery disease (CAD) or myocardial infarction (MI). BACKGROUND: Impaired fibrinolytic function has been associated with CAD and MI. Plasminogen activator inhibitor-1 plays a central role in intravascular thrombosis and thrombolysis; the common insertion/deletion polymorphism (4G/5G) of PAI-1 has been correlated with altered PAI-1 levels and proposed as a coronary risk factor. METHODS: Blood was drawn and DNA extracted from 1,353 consenting patients undergoing coronary angiography. The 4G and 5G alleles of PAI-1 were amplified using specific primers. Amplified products were visualized by staining with ethidium bromide after electrophoresis in 1.5% agarose. RESULTS: Patient age averaged 63.5 (SD 11.7) years; 70% were men, 28% had a history of MI, 66% had severe CAD (>60% stenosis), and 23% had no CAD or MI. Overall, the frequency of the 4G allele was 54.2%, and 78% of patients were 4G carriers. Genotypic distributions were: 4G/4G = 30.1%, 4G/5G = 47.9%, and 5G/5G = 21.8%. Neither carriage of 4G (CAD odds ratio [OR] = 1.08 [0.80 to 1.46], MI OR = 1.11 [0.83 to 1.49]) nor 4G/4G homozygosity (CAD OR = 1.07, MI OR = 0.98) was associated with CAD or MI. In multivariate analyses, risk factors associated with CAD were (in order): gender, age, smoking, diabetes, cholesterol, and hypertension; for MI, they were gender, smoking, and cholesterol. CONCLUSIONS: A common PAI-1 polymorphism (4G) was not importantly associated with angiographic CAD or history of MI in a Caucasian population. Modest risk (i.e., OR <1.5), especially for MI, or risk in association with other factors, cannot be excluded.

Association of lipoprotein lipase gene polymorphisms with coronary artery disease.

OBJECTIVES: The purpose of this study was to test whether the HindIII (+) and PvuII (-) or (+) restriction enzyme-defined alleles are associated with angiographic coronary artery disease (CAD). BACKGROUND: Lipoprotein lipase (LPL) plays a central role in lipid metabolism, hydrolyzing triglyceride in chylomicrons and very low density lipoproteins. Polymorphic variants of the LPL gene are common and might affect risk of CAD. METHODS: Blood was drawn from 725 patients undergoing coronary angiography. Leukocyte deoxyribonucleic acid segments containing the genomic sites were amplified by the polymerase chain reaction and digested, and polymorphisms were identified after electrophoresis in 1.5% agarose gel. RESULTS: In no-CAD control subjects (n = 168), HindIII (-) and (+) allelic frequencies were 28.6% and 71.4%, and (-) and (+) alleles were carried by 44.0% and 86.9% of subjects, respectively. Control PvuII (-) and (+) allelic frequencies were 41.7% and 58.3%, and (-) and (+) alleles were carried by 64.3% and 81.0%, respectively. In CAD patients (>60% stenosis; n = 483), HindIII (+) allelic carriage was increased (93.8% of patients, odds ratio [OR] = 2.28, confidence interval [CI] 1.27 to 4.00). Also, PvuII (-) allelic carriage tended to be more frequent in CAD patients (OR = 1.33, CI 0.92 to 1.93). Adjusted for six CAD risk factors and the other polymorphism, HindIII (+) carriage was associated with an OR = 2.86, CI 1.50 to 5.42, p = 0.0014, and PvulI (-) carriage, OR = 1.42, CI 0.95 to 2.12, p = 0.09. The two polymorphisms were in strong linkage disequilibrium, and a haplotype association was suggested. CONCLUSIONS: The common LPL polymorphic allele, HindIII (+), is moderately associated with CAD, and the PvuII (-) allele is modestly associated (trend). Genetic variants of LPL deserve further evaluation as risk factors for CAD.

Associations between a polymorphism in the gene encoding glycoprotein IIIa and myocardial infarction or coronary artery disease.

OBJECTIVES: The purpose of this study was to determine whether a common variant (PIA2) of the membrane glycoprotein (GP) IIIa gene is associated with myocardial infarction (MI) or coronary artery disease (CAD). BACKGROUND: Platelet GP IIb/IIIa is believed to play a central role in MI, binding fibrinogen, cross-linking platelets and initiating thrombus formation. Genetically determined differences in binding properties of GP IIb/IIIa might result in changes in platelet activation or aggregation and affect the risk of MI or CAD. METHODS: To determine associations (odds ratios [OR] > or =1.5 to 2.0) of genotype with MI or CAD, blood was drawn from 791 patients (pt) undergoing angiography. A 266 base pair fragment of the GP IIIa gene was amplified by the polymerase chain reaction and digested with the MspI restriction enzyme. Genotypes were identified after electrophoresis of digestion products in 1.5% agarose gel. RESULTS: Of the 791 pt, 225 had acute (n = 143) or previous MI, and 276 did not have MI or unstable angina. The PI(A2) allele was carried by 33.8% of MI pt versus 26.9% of no-MI control subjects, OR = 1.39 (95% CI, 0.95 to 2.04, p = 0.09). Angiographically, 549 pt had severe (>60% coronary stenosis) CAD, and 170 had normal coronary arteries (<10% stenosis). The PI(A2) allele was found in 31.0% of CAD pt versus 28.2% of no-CAD control subjects, OR = 1.14 (CI, 0.78 to 1.67, p = 0.50). When adjusted for six standard risk factors, ORs were 1.47 (CI, 0.98 to 2.20, p = 0.062) for MI and 1.20 (CI, 0.80 to 1.81, p = 0.38) for CAD. CONCLUSIONS: The PI(A2) variant of the gene encoding GP IIIa is modestly associated (OR approximately 1.5) with nonfatal MI but shows little if any association with CAD per se.

Implementation of a computerized cardiovascular information system in a private hospital setting.

BACKGROUND: The use of clinical databases improves quality of care, reduces operating costs, helps secure managed care contracts, and assists in clinical research. Because of the large physician input required to maintain these systems, private institutions have often found them difficult to implement. At LDS Hospital in Salt Lake City, Utah, we developed a cardiovascular information system (LDS-CIS) patterned after the Duke University Cardiovascular Database and designed for ease of use in a private hospital setting. METHODS: Features of the LDS-CIS include concise single-page report forms, a relational database engine that is easily queried, automatic generation of final procedure reports, and merging of all data with the hospital's existing information system. So far, data from more than 14,000 patients have been entered. RESULTS: LDS-CIS provides access to data for research to improve patient care. For example, by using data generated by LDS-CIS, the policy requiring surgical backup during percutaneous transluminal coronary angioplasty was eliminated, resulting in no increased patient risk while saving nearly $1 million in 1 year. LDS-CIS generates physician feedback reports documenting performance compared with peers. This physician self-evaluation has standardized and improved care. Information from LDS-CIS has been instrumental in securing and maintaining managed care contracts. LDS-CIS risk analysis provides physicians with outcomes data specific to their current patient's demographics and level of disease to assist in point of care decisions. CONCLUSION: The use of LDS-CIS in the routine operations of LDS Hospital heart services has been found to be feasible, beneficial, and cost-effective.

Angiotensin-converting enzyme genotypes and risk for myocardial infarction in women.

OBJECTIVES: We tested for an association between the angiotensin-converting enzyme (ACE) DD polymorphic genotype and myocardial infarction (MI) in a sample group composed exclusively of women. BACKGROUND: The human ACE gene occurs with either an insertion (I allele) or a deletion (D allele) of a 287-base pair (bp) Alu element. Part of the variance in serum ACE levels may be accounted for by this polymorphism. Also, the DD genotype has been associated with an increased risk of MI in predominantly male populations. However, the risk in women is poorly defined. METHODS: Genomic DNA was extracted from buffy coat blood using a phenol/chloroform method. Angiotensin-converting enzyme alleles were identified using primers to bracket the insertion region in intron 16. Amplification using polymerase chain reaction allowed identification of a 490-bp (I allele) or a 190-bp (D allele) product, or both. RESULTS: Allelic and genotypic frequencies in control subjects were similar to those reported in mostly male populations, and frequencies of genotypes were in the Hardy-Weinberg equilibrium. In contrast, the distribution of genotypes in patients with MI diverged from the equilibrium. Specifically, DD genotypic frequency was increased in women with (n = 141) versus without (n = 338) a previous MI (39% vs. 29%, odds ratio [OR] 1.54, 95% confidence interval 1.02 to 2.32, p < 0.04). Risk was particularly increased in women <60 years old (OR 2.04, p < 0.05). In contrast, the DD genotype did not predict angiographic coronary artery disease. CONCLUSIONS: Consistent with findings in male-dominated populations, a modest association of the ACE DD genotype with MI was found in women. The basis for this association requires further study.

A mutation in the methylenetetrahydrofolate reductase gene is not associated with increased risk for coronary artery disease or myocardial infarction.

OBJECTIVES: We sought to determine whether the C677T transition in the methylenetetrahydrofolate reductase (MTHFR) gene is associated with increased risk for coronary artery disease (CAD) or myocardial infarction (MI). BACKGROUND: Elevated plasma homocysteine has been identified as a risk factor for coronary atherosclerosis. Homocysteinemia may result from deficient MTHFR activity. A thermolabile form of MTHFR, associated with a C677T genetic transition, shows reduced activity and may be a risk factor for CAD. METHODS: Blood was withdrawn from patients undergoing coronary angiography, and DNA was extracted by a phenol-chloroform method. Genotyping was done by polymerase chain reaction (PCR) amplification of a 198-base pair segment of the MTHFR gene that brackets nucleotide 677. The amplicon was digested with the HinfI restriction enzyme. Products were visualized after electrophoresis in 1.5% agarose with ethidium bromide. RESULTS: Among 200 patients with a diagnosis of MI, the polymorphic allelic frequency was 33.3%, compared with 32.1% among 554 control subjects (p = 0.68); homozygosity was present in 11.5% of patients and 10.6% of control subjects (p = 0.74, odds ratio [OR] 1.09, 95% confidence interval [CI] 0.63 to 1.82). Among 510 patients with severe CAD (>60% stenosis), allelic frequency was 32.0%, compared with 34.8% for 168 subjects without CAD (<10% stenosis, p = 0.33); 11.2% of patients with CAD compared with 13.1% of control subjects were homozygous (p = 0.50, OR 0.83, 95% CI 0.5 to 1.40). CONCLUSIONS: Patients with angiographic evidence of CAD or clinical MI do not show an increased frequency of the C677T transition in the MTHFR gene. Our findings do not support this polymorphism as a risk factor for CAD or MI in a predominantly white, well nourished population of unrestricted age.

Automated management of screening and diagnostic mammography.

We designed an automated system for managing large-scale screening and diagnostic mammography. The system collects coded mammographic findings from the radiologist and records a history directly from the patient. This information is stored in an integrated clinical data base to which the results of subsequent examinations or surgery are added. In addition, the system generates letters to the patient and her physician that describe mammographic findings and letters reminding them of routine screening visits. For patients who have positive results on examinations, it checks for records of biopsy or repeat mammography and generates follow-up letters if appropriate intervention is not found. While this system is part of a comprehensive computerized hospital information system, mammography management tools with most of the features described can be designed for relatively inexpensive microcomputers.