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Hospitals can create educational materials to help doctors comply with practice guidelines for the treatment of heart attack. Practice guidelines are documents that recommend the best treatments for specific conditions based on scientific evidence., Context: Quality of care of patients with acute myocardial infarction (AMI) has received intense attention. However, it is unknown if a structured initiative for improving care of patients with AMI can be effectively implemented at a wide variety of hospitals. Objective: To measure the effects of a quality improvement project on adherence to evidence-based therapies for patients with AMI. Design and Setting: The Guidelines Applied in Practice (GAP) quality improvement project, which consisted of baseline measurement, implementation of improvement strategies, and re-measurement, in 10 acute-care hospitals in southeast Michigan. Patients: A random sample of Medicare and non-Medicare patients at baseline (July 1998-June 1999; n = 735) and following intervention (September 1-December 15,2000; n=914) admitted at the 10 study centers for treatment of confirmed AMI. A random sample of Medicare patients at baseline (January-December 1998; n=513) and at re-measurement (March-August 2001; n=388) admitted to 11 hospitals that volunteered, but were not selected, served as a control group. Intervention: The GAP project consisted of a kickoff presentation; creation of customized, guideline-oriented tools designed to facilitate adherence to key quality indicators; identification and assignment of local physician and nurse opinion leaders; grand rounds site visits; and premeasurement and postmeasurement of quality indicators. Main Outcome Measures: Differences in adherence to quality indicators (use of aspirin, [beta]-blockers, and angiotensin-converting enzyme [ACE] inhibitors at discharge; time to reperfusion; smoking cessation and diet counseling; and cholesterol assessment and treatment in ideal patients, compared between baseline and postintervention samples and among Medicare patients in GAP hospitals and the control group. Results: Increases in adherence to key treatments were seen in the administration of aspirin (81% vs 87%; p=.02) and [beta]-blockers (65% vs 74%; p=.04) on admission and use of aspirin (84% vs 92%; P=.002) and smoking cessation counseling (53% vs 65%; P = .02) at discharge. For most of the other indicators, nonsignificant but favorable trends toward improvement in adherence to treatment goals were observed. Compared with the control group, Medicare patients in GAP hospitals showed a significant increase in the use of aspirin at discharge (5% vs 10%; P Conclusions: Implementation of guideline-based tools for AMI may facilitate quality improvement among a variety of institutions, patients, and caregivers. This initial project provides a foundation for future initiatives aimed at quality improvement.

Ventricular tachycardia (VT), or the tendency of the ventricle (a chamber of the heart) to contract at an excessively fast rate, is an arrhythmic disorder that can lead to cardiac death. The tachycardia can be caused by several different processes occurring in the cardiac muscle, and the exact mechanism leading to the arrhythmia generally determines the choice of medication used to treat it. One pharmacological approach to arrythmia is the administration of beta blockers (drugs that block the actions of epinephrine). A study was conducted to assess the role of beta blockade therapy in the treatment of different types of arrhythmias. Fourteen patients with chronic VT were evaluated. VT was induced by the administration of isoproterenol (a drug that mimics some of the effects of epinephrine) or electrical stimulation of the heart (done by means of electrodes inserted via the femoral vein). VT was caused by one of three mechanisms: enhanced automaticity (an increase in the intrinsic rate of ventricular contraction), triggered automaticity (a similar increase induced by electrical stimulation), and reentry (very rapid bursts of contraction of the heart following electrical stimulation). The beta blocker propranolol was administered alone or in combination with other classes of anti-arrhythmic drugs. Propranolol alone was effective in preventing VT in the group of patients in whom VT resulted from enhanced automaticity; the other two groups required combined treatment. Beta blockers are effective as anti-arrhythmic agents only for patients in whom VT results from enhanced automaticity. (Consumer Summary produced by Reliance Medical Information, Inc.)

The basal forebrain (BF) plays an important role in the control of cortical activation and attention. Understanding the modulation of BF neuronal activity is a prerequisite to treat disorders of cortical activation involving BF dysfunction, such as Alzheimer's disease. Here we reveal the interaction between cholinergic neurons and cortically projecting BF GABAergic neurons using immunohistochemistry and whole-cell recordings in vitro. In GAD67-GFP knock-in mice, BF cholinergic (choline acetyltransferase-positive) neurons were intermingled with GABAergic (GFP+) neurons. Immunohistochemistry for the vesicular acetylcholine transporter showed that cholinergic fibers apposed putative cortically projecting GABAergic neurons containing parvalbumin (PV). In coronal BF slices from GAD67-GFP knock-in or PV-td Tomato mice, pharmacological activation of cholinergic receptors with bath application of carbachol increased the firing rate of large (>20 μm diameter) BF GFP+ and PV (tdTomato) neurons, which exhibited the intrinsic membrane properties of cortically projecting neurons. The excitatory effect of carbachol was blocked by antagonists of M1 and M3 muscarinic receptors in two subpopulations of BF GABAergic neurons [large hyperpolarization-activated cation current (Ih ) and small Ih, respectively]. Ion substitution experiments and reversal potential measurements suggested that the carbachol-induced inward current was mediated mainly by sodium-permeable cation channels. Carbachol also increased the frequency of spontaneous excitatory and inhibitory synaptic currents. Furthermore, optogenetic stimulation of cholinergic neurons/fibers caused a mecamylamine- and atropine-sensitive inward current in putative GABAergic neurons. Thus, cortically projecting, BF GABAergic/PV neurons are excited by neighboring BF and/or brainstem cholinergic neurons. Loss of cholinergic neurons in Alzheimer's disease may impair cortical activation, in part, through disfacilitation of BF cortically projecting GABAergic/PV neurons. [ABSTRACT FROM AUTHOR]

The prevention of pacemaker-mediated tachycardias requires a safe, reliable method for distinguishing retrograde from anterograde atrial activation by dual chamber pacemakers. In this study, a technique was developed to detect the morphological change that occurs in the waveform of the intro-atrial electrogram during retrograde atrial activation. The method employed for waveform analysis is hosed upon statistical correlation. In 19 patients undergoing electrophysiological studies, atrial electrograms were recorded from bipolar endocardial electrodes during sinus rhythm and 1:1 retrograde atrial depolarization while undergoing right ventricular pacing. Data were digitally sampled at 750, 1,000, and 1,500 Hz. Templates of anterograde atrial depolarization were constructed by signal averaging waveforms from an in Dial sinus rhythm passage. These were used for analysis of anterograde depolarizations from a subsequent passage of sinus rhythm and a passage of known retrograde atrial depolarization. In all 19 cases, a patient-specific threshold could be derived to separate anterograde from retrograde atrial depolarizations using 1,000 Hz and 1,500 Hz sampling rates. However, at a sampling rate of 750 Hz, separation of anterograde from retrograde atrial activation was possible in only 16/19 patients (84%). We conclude that correlation waveform analysis of a suitably sampled atrial electrogram is a reliable method of discriminating retrograde atrial depolarization from anterograde atrial depolarization in intracardiac electrograms. [ABSTRACT FROM AUTHOR]