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Background Commonly used cardiovascular risk calculators do not provide risk estimation of stroke, a major postoperative complication with high morbidity and mortality. We developed and validated an accurate cardiovascular risk prediction tool for stroke, major cardiac complications (myocardial infarction or cardiac arrest), and mortality after non-cardiac surgery. Methods and Results This retrospective cohort study included 1 165 750 surgical patients over a 4-year period (2007-2010) from the American College of Surgeons National Surgical Quality Improvement Program Database. A predictive model was developed with the following preoperative conditions: age, history of coronary artery disease, history of stroke, emergency surgery, preoperative serum sodium (≤130 mEq/L, >146 mEq/L), creatinine >1.8 mg/dL, hematocrit ≤27%, American Society of Anesthesiologists physical status class, and type of surgery. The model was trained using American College of Surgeons National Surgical Quality Improvement Program data from 2007 to 2009 (n=809 880) and tested using data from 2010 (n=355 870). Risk models were developed using multivariate logistic regression. The outcomes were postoperative 30-day stroke, major cardiovascular events (myocardial infarction, cardiac arrest, or stroke), and 30-day mortality. Major cardiac complications occurred in 0.66% (n=5332) of patients (myocardial infarction, 0.28%; cardiac arrest, 0.41%), postoperative stroke in 0.25% (n=2005); 30-day mortality was 1.66% (n=13 484). The risk prediction model had high predictive accuracy with area under the receiver operating characteristic curve for stroke (training cohort=0.869, validation cohort=0.876), major cardiovascular events (training cohort=0.871, validation cohort=0.868), and 30-day mortality (training cohort=0.922, validation cohort=0.925). Surgery types, history of stroke, and coronary artery disease are significant risk factors for stroke and major cardiac complications. Conclusions Postoperative stroke, major cardiac complications, and 30-day mortality can be predicted with high accuracy using this web-based predictive model.

We studied the molecular bases for C8 beta deficiency in 34 unrelated families from the United States and the former Soviet Union. These families represented 69 unrelated null alleles of which 59 (86%) were found to be due to a previously described C-->T transition in exon 9. Six additional null alleles were also caused by C-->T transitions, of which four (6%) were located at base 388 in exon 3, one (2%) at base 298 in exon 3, and one (2%) involved cytosine 847 in exon 6. All of the null alleles affecting cytosine 388 were linked to the sequence polymorphism at base 376, which determines the uncommon C8 beta acidic allotype. Two null alleles were caused by single base pair deletions of cytosines at positions 430 and 632 in exons 3 and 5, respectively. Of the characterized null alleles, 97% were due to C-->T transitions in which an arginine (64 alleles) or a glutamine (one allele) was replaced by a stop codon. The basis for this apparent high frequency of C-->T transitions occurring in a relatively short stretch of DNA is uncertain.