Retrospective Comparison of Cardiac Testing and Results on Inpatients with Low Pretest Probability Compared with Moderate/High Pretest Probability for Coronary Artery Disease.

OBJECTIVE: To determine whether admission, and provocative stress testing of patients who have ruled out for acute coronary syndrome put patients with low-risk category for coronary artery disease (CAD) at risk for false-positive provocative stress testing and unnecessary coronary angiogram/imaging. METHODS: A retrospective chart review was performed on patients between 30 and 70 years old, with no pre-existing diagnosis of CAD, admitted to observation or inpatient status chest pain or related complaints. Included patients were categorized based on Duke Clinical Score for pretest probability for CAD into either low-risk group, or moderate/high-risk group. The inpatient course was compared including whether provocative stress testing was performed; results of stress testing; whether patients underwent further coronary imaging; and what the results of the further imaging showed. RESULTS: 543 patients were eligible: 305 low pretest probability, and 238 moderate/high pretest probability. No difference was found in rate of stress testing relative risk (RR) = 1.01 (95% CI, 0.852 to 1.192; P = 0); rate of positive or equivocal stress tests between the 2 groups: RR = 0.653 (95% CI, 0.415 to 1.028; P = .07,). Low-pretest-probability patients had a lower likelihood of positive coronary imaging after stress test, RR = 0.061 (95% CI, 0.004 to 0.957; P = .001). CONCLUSION: Follow-up provocative testing of all patients admitted/observed after emergency department presentation with chest pain is unlikely to find CAD in patients with low pretest probability. Testing all low-probability patients puts them at increased risk for unnecessary invasive confirmatory testing. Further prospective testing is needed to confirm these retrospective results.

Decreasing hormonal promotion is key to breast cancer prevention.

An early full-term pregnancy in women is highly protective against breast cancer. This protection can be mimicked by short-term treatment with estradiol plus progesterone in nulliparous rats. We determined the effect of long-term hormonal promotion following the protective short-term estradiol and progesterone treatment that mimics parity protection against mammary tumors. Rats were treated with N-methyl-N-nitrosourea before or after protective hormone treatment. In brief, the animals could be broadly classified into three categories. First, the controls that received no protective hormone treatment, second, the short-term protective hormone treated rats, and third, rats which received the short-term protective hormone treatment plus continuous treatment with estradiol or progesterone or a combination of estradiol and progesterone. Different doses of hormones were used for short-term protective and long-term promotion treatments. The experiments were terminated 9 months post carcinogen treatment. Mammary tumor incidence in all the short-term estradiol- plus progesterone-treated rats was significantly lower compared with controls. Short-term hormone treatment followed by long-term promotion resulted in an increased mammary tumor incidence compared with animals that received only the short-term treatment. Overall, the results demonstrate the importance of the promotional environment in mammary carcinogenesis indicating that the decreased promotional environment could be the reason for protection against mammary carcinogenesis.