PubMed · 9751602
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J L Vincent, J Berré. 1998. Beta-blocking agents can increase PaO2.. https://doi.org/10.1097/00003246-199809000-00037
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OBJECTIVES: The goal of this study was to determine how often atrioventricular (AV) block is really caused by medications. BACKGROUND: Beta-blockers, verapamil, and diltiazem are considered a cause of AV block for which pacemaker implantation is not indicated. However, it is not known if such patients can expect a benign course after discontinuation of the culprit medication. METHODS: Consecutive patients with II or III degree AV block not related to acute myocardial infarction, digitalis toxicity, or vasovagal syncope were studied. The level of AV block (AV-nodal or infranodal) was defined by electrocardiographic criteria. The cause and effect relation between AV block and drugs was defined according to the response to drug discontinuation. RESULTS: Of 169 patients with AV block, 92 (54%) were receiving beta-blockers and/or verapamil or diltiazem. Patients receiving medications had similar clinical and electrocardiographic characteristics with patients who had AV block in the absence of drugs. Drug discontinuation was followed by resolution of AV block in 41% of cases, whereas spontaneous improvement of AV conduction occurred in 23% of patients who had AV block in the absence of drugs. However, 56% of the patients for whom drug discontinuation led to resolution of AV block had recurrence of AV block in the absence of therapy. Atrioventricular block that was "truly caused by drugs" was found in only 15% of patients who had II or III degree AV block during therapy with beta-blockers, verapamil, or diltiazem. CONCLUSIONS: Atrioventricular block is commonly "related to drugs" but is rarely "caused by drugs."
OBJECTIVES: The purpose of this study was to determine whether state-mandated continuing medical education (CME) requirements affect the use of evidence-based therapies and outcomes in patients with acute myocardial infarction (AMI). BACKGROUND: The Institute of Medicine recommends that educational programs demonstrate their effect through process and outcome measures. METHODS: We analyzed 134,609 patients according to whether or not CME was mandated in the state of physician practice. A hierarchical multivariable model was developed that controlled for state, hospital, physician, and patient level characteristics to determine the association between state CME requirements and the use of evidence-based therapies. Primary outcome measures were admission aspirin use and reperfusion therapy, and discharge aspirin and beta-blocker prescription. Thirty-day and one-year mortality were secondary outcome measures. RESULTS: States with and without CME requirements had similar rates of aspirin use at admission and discharge (79.9% vs. 79.4% and 72.5% vs. 72.5%, respectively) and beta-blocker prescription at discharge (53.6% vs. 55.3%). The rate of reperfusion therapy at admission was significantly higher in states requiring CME (53.1%) compared with states without CME (47.9%) (p < 0.0001). After adjustment, patients admitted in CME-requiring states were significantly more likely to receive reperfusion therapy, mainly owing to "patented" thrombolytic therapy (odds ratio 1.15; p = 0.016). There was no association between CME requirements and one-year mortality. CONCLUSIONS: State-mandated CME had little association with AMI care or outcome, other than an increased use of patented thrombolytic therapy. Further research is needed to maximize the measurable effect of CME on the use of proven therapies irrespective of whether patented or generic medications are involved.
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