High-Sensitivity Troponin I after Cardiac Surgery and 30-Day Mortality.

BACKGROUND: Consensus recommendations regarding the threshold levels of cardiac troponin elevations for the definition of perioperative myocardial infarction and clinically important periprocedural myocardial injury in patients undergoing cardiac surgery range widely (from >10 times to ≥70 times the upper reference limit for the assay). Limited evidence is available to support these recommendations. METHODS: We undertook an international prospective cohort study involving patients 18 years of age or older who underwent cardiac surgery. High-sensitivity cardiac troponin I measurements (upper reference limit, 26 ng per liter) were obtained 3 to 12 hours after surgery and on days 1, 2, and 3 after surgery. We performed Cox analyses using a regression spline that explored the relationship between peak troponin measurements and 30-day mortality, adjusting for scores on the European System for Cardiac Operative Risk Evaluation II (which estimates the risk of death after cardiac surgery on the basis of 18 variables, including age and sex). RESULTS: Of 13,862 patients included in the study, 296 (2.1%) died within 30 days after surgery. Among patients who underwent isolated coronary-artery bypass grafting or aortic-valve replacement or repair, the threshold troponin level, measured within 1 day after surgery, that was associated with an adjusted hazard ratio of more than 1.00 for death within 30 days was 5670 ng per liter (95% confidence interval [CI], 1045 to 8260), a level 218 times the upper reference limit. Among patients who underwent other cardiac surgery, the corresponding threshold troponin level was 12,981 ng per liter (95% CI, 2673 to 16,591), a level 499 times the upper reference limit. CONCLUSIONS: The levels of high-sensitivity troponin I after cardiac surgery that were associated with an increased risk of death within 30 days were substantially higher than levels currently recommended to define clinically important periprocedural myocardial injury. (Funded by the Canadian Institutes of Health Research and others; VISION Cardiac Surgery ClinicalTrials.gov number, NCT01842568.).

Summer syncope syndrome redux.

BACKGROUND: While antihypertensive therapy is known to reduce the risk for heart failure, myocardial infarction, and stroke, it can often cause orthostatic hypotension and syncope, especially in the setting of polypharmacy and possibly, a hot and dry climate. The objective of the present study was to investigate whether the results of our prior study involving continued use of antihypertensive drugs at the same dosage in the summer as in the winter months for patients living in the Sonoran desert resulted in an increase in syncopal episodes during the hot summer months. METHODS: All hypertensive patients who were treated with medications and admitted with International Classification of Diseases, 9th Revision code diagnosis of syncope were included. This is a 3-year retrospective chart review study. They were defined as "cases" if they presented during the summer months (May to September) and "controls" if they presented during the winter months (November to March). The primary outcome measure was the presence of clinical dehydration. The statistical significance was determined using the 2-sided Fisher's exact test. RESULTS: A total of 834 patients with an International Classification of Diseases, 9th Revision code diagnosis of syncope were screened: 477 in the summer months and 357 in the winter months. In patients taking antihypertensive medications, there was a significantly higher number of cases of syncope secondary to dehydration during the summer months (40.5%) compared with the winter months (29%) (P = .04). No difference was observed in the type of antihypertensive medication used and syncope rate. The number of antihypertensives used did not increase the cases of syncope in either summer or winter. CONCLUSIONS: An increased number of syncope events was observed in the summer months among people who reside in a dry desert climate and who are taking antihypertensive medications. The data confirm our earlier observations that demonstrated a greater number of cases of syncope among people who reside in a dry desert climate who were taking antihypertensive medications during summer months. We recommend judicious reduction of antihypertensive therapy in patients residing in a hot and dry climate, particularly during the summer months.

The epidemic of the 20(th) century: coronary heart disease.

Heart disease was an uncommon cause of death in the US at the beginning of the 20th century. By mid-century it had become the commonest cause. After peaking in the mid-1960s, the number of heart disease deaths began a marked decline that has persisted to the present. The increase in heart disease deaths from the early 20th century until the 1960s was due to an increase in the prevalence of coronary atherosclerosis with resultant coronary heart disease, as documented by autopsy studies. This increase was associated with an increase in smoking and dietary changes leading to an increase in serum cholesterol levels. In addition, the ability to diagnose acute myocardial infarction with the aid of the electrocardiogram increased the recognition of coronary heart disease before death. The substantial decrease in coronary heart disease deaths after the mid-1960s is best explained by the decreased incidence, and case fatality rate, of acute myocardial infarction and a decrease in out-of-hospital sudden coronary heart disease deaths. These decreases are very likely explained by a decrease in coronary atherosclerosis due to primary prevention, and a decrease in the progression of nonobstructive coronary atherosclerosis to obstructive coronary heart disease due to efforts of primary and secondary prevention. In addition, more effective treatment of patients hospitalized with acute myocardial infarction has led to a substantial decrease in deaths due to acute myocardial infarction. It is very likely that the 20th century was the only century in which heart disease was the most common cause of death in America.

A medical education as an investment: financial food for thought.

Every year that the training period can be shortened increases the value of a medical education. Tuition covers only a fraction of the cost of medical education, making the societal investment in older students less financially robust. Shortening training periods would immediately solve the shortage of residency training positions. With a few exceptions, a medical education is a good investment for women. We are skeptical of the proposals to address the skyrocketing student debt because they do not confront the primary problem. The best way to minimize debt is thrift, and the best way to make a career in medicine more desirable is to shorten the training time.