Effectiveness of the electronic medical record in cholesterol management in patients with coronary artery disease (Virtual Lipid Clinic).

This study demonstrates that the Virtual Lipid Clinic, an electronic medical record with computer-assisted cholesterol management, is associated with improved lipid management in patients with coronary artery disease. In comparison to traditional documentation methods with "pen and paper" charts, outpatient visits utilizing the electronic medical record were associated with a twofold increase in low-density lipoprotein (LDL) documentation, a threefold increase in achieving LDL goal, and a 30% increase in the use of lipid-lowering drugs.

Electrophysiologic testing to identify patients with coronary artery disease who are at risk for sudden death. Multicenter Unsustained Tachycardia Trial Investigators.

BACKGROUND: The mortality rate among patients with coronary artery disease, abnormal ventricular function, and unsustained ventricular tachycardia is high. The usefulness of electrophysiologic testing for risk stratification in these patients is unclear. METHODS: We performed electrophysiologic testing in patients who had coronary artery disease, a left ventricular ejection fraction of 40 percent or less, and asymptomatic, unsustained ventricular tachycardia. Patients in whom sustained ventricular tachyarrhythmias could be induced were randomly assigned to receive either antiarrhythmic therapy guided by electrophysiologic testing or no antiarrhythmic therapy. The primary end point was cardiac arrest or death from arrhythmia. Patients without inducible tachyarrhythmias were followed in a registry. We compared the outcomes of 1397 patients in the registry with those of 353 patients with inducible tachyarrhythmias who were randomly assigned to receive no antiarrhythmic therapy in order to assess the prognostic value of electrophysiologic testing. RESULTS: Patients were followed for a median of 39 months. In a Kaplan-Meier analysis, two-year and five-year rates of cardiac arrest or death due to arrhythmia were 12 and 24 percent, respectively, among the patients in the registry, as compared with 18 and 32 percent among the patients with inducible tachyarrhythmias who were assigned to no antiarrhythmic therapy (adjusted P<0.001). Overall mortality after five years was 48 percent among the patients with inducible tachyarrhythmias, as compared with 44 percent among the patients in the registry (adjusted P=0.005). Deaths among patients without inducible tachyarrhythmias were less likely to be classified as due to arrhythmia than those among patients with inducible tachyarrhythmias (45 and 54 percent, respectively; P=0.06). CONCLUSIONS: Patients with coronary artery disease, left ventricular dysfunction, and asymptomatic, unsustained ventricular tachycardia in whom sustained ventricular tachyarrhythmias cannot be induced have a significantly lower risk of sudden death or cardiac arrest and lower overall mortality than similar patients with inducible sustained tachyarrhythmias.

Turbulence intensity in aortic stenosis: frequency characteristics and effects of alterations in left ventricular function.

Turbulent blood flow can occur downstream from a stenosis. The purpose of this study was to quantitate turbulence intensity and its frequency characteristics in the ascending aorta in adult patients with and without valvular stenosis, and to use extrasystoles to analyze the effects of changes in left ventricular function on turbulence. Turbulence intensity was determined from the digitized, high frequency oscillations seen in high fidelity pressure recordings of 25 patients with valvular aortic stenosis. The intensity of turbulence was quantitated as the root-mean-square (mmHg) of pressure fluctuations and as the total spectral power (mmHg2/beat) of the frequency spectrum between 25 Hz and 400 Hz. Frequency characteristics were summarized by the mean and median frequency of spectral power and partitioning the spectrum into 25 Hz segments. Ten adult patients without aortic valve or outflow tract abnormalities served as controls. Adult patients with aortic stenosis had significantly more turbulence in the ascending aorta than controls (total spectral power 1577 +/- 450 mmHg2 vs. 198 +/- 22 mmHg2, p < 0.01). Furthermore, the frequency distribution in aortic stenosis was biased towards higher frequencies (mean frequency 35 +/- 14 Hz vs 54 +/- 2 Hz, p < 0.001). Turbulence intensity in aortic stenosis demonstrated beat to beat modulation by left ventricular function. The total spectral power of a sinus beat was 1888 +/- 762 mmHg2, and fell to 137 +/- 63 mmHg2 in a weak premature beat, and rose to 3618 +/- 1178 mmHg2 in a potentiated post- extrasystolic beat (p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Permanent pacemaker implantation in the cardiac catheterization laboratory versus the operating room: an analysis of hospital charges and complications.

Permanent pacemakers may be implanted in operating rooms, special procedure laboratories, or cardiac catheterization laboratories. Previous investigators have shown no difference in efficacy or complications in the operating room versus the cardiac catheterization laboratory. We retrospectively analyzed the hospital bills of 30 patients undergoing permanent pacemaker implantation at our institution. Group I was 15 consecutive patients implanted in the operating room and group II was 15 consecutive patients implanted in the cardiac catheterization laboratory, all by the same operators. Hospital charges that were specific to the site of implantation were analyzed. Physician charges for implantation, anesthesiologist, and radiologist charges were not analyzed. There were no in-hospital complications in either group. The mean charges for group I were $1,856.00 and group II were $1,075.00 (P < 0.001). We conclude that implantation of permanent pacemakers in the cardiac catheterization laboratory is associated with significantly lower hospital charges compared to implantation in the operating room and has an equally low complication rate.

A technique utilizing a steerable hydrophilic guidewire for permanent pacemaker implantation.

We report the use of a steerable hydrophilic guidewire for permanent pacemaker implantation. This wire, previously used for peripheral vascular and cardiac angiography, is able to be steered and passed in many situations when a standard guidewire cannot be used. We report three cases where the standard J-tipped guidewire could not be passed by either the cephalic or subclavian route and the hydrophilic guidewire allowed for successful atraumatic placement of a sheath and pacemaker lead.

The safety and efficacy of chronic ventricular pacing at 1.6 volts using a steroid eluting lead.

Steroid eluting leads may allow for lower chronic pacing thresholds and therefore lower pacing outputs. Twenty-two patients (15 presenting with syncope) were implanted with VVI or VVIR pacemakers and transvenous steroid eluting leads and followed for a mean of 20.6 months while being paced at 1.6 V and 0.6 msec. Mean acute voltage pacing thresholds were 0.40 V at 0.5 msec and chronic pulse width thresholds were 0.21 msec at 0.8 V. Pacemaker function was documented with one to three 24-hour Holter monitors, attached during the 2-6 week postimplant period, bimonthly transtelephonic monitoring, and monthly pacemaker clinic visits. No patient developed recurrent symptoms and consistent capture was verified in all patients on every 24-hour Holter recording and transtelephonic monitor. Chronic ventricular pacing at an output of 1.6 V at 0.6 msec is safe and effective when using a steroid eluting lead and potentially has implications for pacemaker longevity.

Noncardiogenic mechanisms of right heart dysfunction.

Alterations in right ventricular (RV) performance are critical to the cardiac dysfunction witnessed in adult respiratory distress syndrome (ARDS), septic shock (SS), and as a consequence of positive end-expiratory pressure (PEEP) administration during mechanical ventilation. The authors review evidence for right heart dysfunction in these circumstances. In ARDS, an increase in RV afterload with the onset of pulmonary artery hypertension is the predominant factor promoting RV dysfunction. In SS, most investigators agree that a primary decrease in myocardial contractility is the major factor limiting RV performance. The application of PEEP during mechanical ventilation can potentiate alterations in RV preload, afterload, and/or contractility, all of which promote RV dysfunction and compromise left ventricular filling. As RV dysfunction may seriously affect global myocardial performance in all of these settings, the clinician must identify that RV function is impaired, discern the contributing mechanism, and select an appropriate therapeutic regimen targeted at addressing this predominant mechanism. Assessment and management strategies are described.

Surgical interruption of postganglionic innervation of the sinoatrial nodal region.

Recent experiments have revealed synapses that selectively mediate right and left vagal regulation of sinoatrial function in the fat pad overlying and surrounding the right pulmonary vein complex. However, precise vagal postganglionic pathways to the sinoatrial region have remained obscure. Such pathways, including critically important neural inputs to sinoatrial and atrioventricular nodal regions, may be vulnerable to surgical approaches to atrial or intracardiac repair. The present experiments seek to delineate specific autonomic pathways to the sinoatrial region of the canine heart. The distal ends of the cut right and left cervical vagi and the right and left ansae subclaviae were electrically stimulated (10 to 20 Hz, 1 msec, 2 to 3 V) before and after surgical incisions were placed. Cut No. 1 was made longitudinally along the ventral caval surface from the pericardial reflection caudally to the pulmonary vein fat pad, cut No. 2 was made from the caudal end of cut No. 1 transversely across the sulcus terminalis to a point midway across the anterior (ventral) surface of the right atrium. Each incision was closed with 4-0 silk, with care being taken to avoid injury to either the sinoatrial nodal or the pulmonary fat pad regions. In four of seven animals, these two incisions totally interrupted vagal input to the sinoatrial node, whereas in the remaining three dogs a residual inhibitory influence remained. These residual fibers were surgically ablated by excision of globular fat pads situated on the rostrodorsal surfaces of the right superior pulmonary vein, suggesting a dorsorostral route into the interatrial septum and thence to the sinoatrial node. There was little or no interruption of either right or left vagal input to the atrioventricular nodal region; sympathetic supplies to both sinoatrial nodal and atrioventricular nodal regions remained essentially intact after the two incisions. Thus the major parasympathetic postganglionic projections to the sinoatrial node in the dog heart are by way of the free wall of the right atrium and are vulnerable to surgical interventions in this portion of the heart.

Parasympathetic postganglionic pathways to the sinoatrial node.

Vagal ganglia that innervate the canine sinoatrial node (SAN) have been localized to a fat pad overlying and surrounding the right pulmonary vein complex (PVFP). The ventral epicardial surface of the right atrium was mapped in seven dogs anesthetized with alpha-chloralose after beta-blockade (timolol) and cardiac sympathetic and parasympathetic decentralization. A small, concentric bipolar exploring electrode was used to stimulate (during the atrial refractory period and using trains of five to eight stimuli per beat) systematically in the epicardial regions between the PVFP and the SAN. Changes in SAN rate with stimulation were measured, and the anatomic location was identified on a 150-point grid fitted to conform to size and shape of the atrium. Mapping was performed before and after local (PVFP) and systemic ganglionic blockade (hexamethonium). Data reveal that the primary vagal postganglionic pathways to the sinoatrial nodal region are subepicardial and adjacent to the SAN artery along the sulcus terminalis. Hexamethonium in the PVFP abolishes SAN inhibition during preganglionic vagal excitation, without interrupting vagal suppression of atrioventricular conduction. However, SAN slowing (with varying attenuation) continued to occur after hexamethonium (either PVFP or systemically) when the exploring electrode was applied directly over intramural postganglionic fibers between PVFP and sinus node. Attention is directed to existence of a very few synapses closer to SAN, probably in isolated ganglia immersed in fatty connective tissues along the sulcus terminalis.

Differential autonomic control of SAN and AVN regions of the canine heart: structure and function.

Both anatomical and physiologic evidence for relatively rich autonomic innervation of sinoatrial (SAN) and atrioventricular (AVN) regions of the canine heart exist, with indication that SAN is especially responsive to parasympathetic, while AVN is preferentially sensitive to sympathetic regulation. The distribution of autonomic pathways are sufficiently separate and discrete that careful surgical intervention can selectively delete either parasympathetic or sympathetic nerve supplies to either (or both) SAN and AVN regions. Selective blockade by restricted injections of lidocaine (general neuronal blocker) or hexamethonium (ganglionic blocker) indicate that the vast majority (perhaps all) of vagal ganglia supplying SAN reside in the pulmonary vein fat pad and associated adipose tissues. In contrast, the vagal ganglia supplying AVN are found within a smaller fat pad overlying epicardium at the junction of inferior vena cava-inferior left atrium. These vagal pathways to either automatic cells of SAN or conductile tissues of AVN can be selectively interrupted without interfering with vagal regulation of the remaining intact system. Electroneurograms from large neurons situated within PVFP of the anesthetized, open-chest animal, reveal vigorous, phasic electrical activity associated with the cardiac and respiratory cycles, as well as with sensory stimulation of the heart, great vessels, and lungs. Spontaneous electrical activity of presently unknown origin is also observed. Direct neuronal stimulation, plus retrograde transport of fluorescent markers suggest that highly selective postganglionic intracardiac pathways may regulate discharge patterns of the sinus automatic cells.

Oscillatory hyperventilation in severe congestive heart failure secondary to idiopathic dilated cardiomyopathy or to ischemic cardiomyopathy.

Thirty-one subjects with chronic congestive heart failure (CHF) were separated into 3 groups according to ventilatory patterns during graded exercise: Group 1--oscillators (n = 6); group 2-intermediate oscillators (n = 14); and group 3--nonoscillators (n = 11). Group 1 patients showed cyclic fluctuations in minute ventilation (change of 30 to 40 liters/min) and arterial PO2 (change of 38.0 +/- 4.1 mm Hg) and PCO2 (change of 11 +/- 2.8 mm Hg). The nadir in arterial PO2 occurred at times when wasted ventilatory effort was maximal. The amplitude of ventilatory oscillations in group 1 patients increased in the transition from rest to light exercise and damped with heavy exercise. There was no evidence of alveolar hypoventilation at the nadirs of minute ventilation; arterial PCO2 was always 40 mm Hg or less. Substantial hyperventilation (ventilatory equivalent for CO2 twice normal) occurred with maximal minute ventilation in group 1 patients. Oscillatory hyperventilation correlated with severity of CHF. Maximal oxygen uptake was significantly lower in group 1 (11.7 +/- 1.1 ml/kg/min) than group 3 (17.9 +/- 1.8 ml/kg/min) (p less than 0.05). Oscillatory hyperventilation during exercise may accompany severe CHF and compounds the inadequate delivery of oxygen by the failing heart.

Functional interdependence of discrete vagal projections to SA and AV nodes.

Dynamic modulation of chronotropic and dromotropic function was evaluated in anesthetized dogs before and after selective parasympathectomy of the atrioventricular (AV) node. Vagal and cardiac sympathetic efferent nerves were decentralized, and the distal cut ends of the cervical vagi were stimulated at frequencies from 1 to 25 Hz with step-wise voltage changes. To investigate parasympathetic modulation of AV conduction, stimulations were performed with and without atrial pacing. After determination of chronotropic and dromotropic responses, in the intact state, selective AV node parasympathectomy was performed as previously described [Am. J. Physiol. 248 (Heart Circ. Physiol. 17): H61-H68, 1985]. Stimulation protocols were then repeated. Control results in intact animals reveal a parallel and finely balanced vagal regulation of chronotropic and dromotropic responses over a wide range of frequency stimulations. Conversely, selective parasympathectomy of the AV node interrupts extrinsic vagal modulation of AV conduction without affecting parasympathetic control of chronotropic function. The dynamic balance of chronotropic and dromotropic function, modulated by extrinsic vagal input, reflects the parallel activation of functionally and anatomically distinct parasympathetic projections to the sinoatrial (SA) and AV nodal tissue. Thus present experiments allow a more detailed examination of vagal innervation of the SA and AV nodes, the importance of their balance through neuroregulation, and progress toward understanding the pathophysiology of disturbances to this balance.

The practical use of porcine xenografting.

The authors present a literature review of porcine grafting and its application at Westside Veterans Administration Medical Center. Porcine xenografts allow wounds that would normally need skin grafting and are slow or nonhealing to close without additional trauma to the patient.

Parallel baroreceptor control of sinoatrial rate and atrioventricular conduction.

The vagal efferent limb of baroreceptor reflexes was studied in 10 anesthetized (alpha-chloralose) dogs to determine its differential regulatory significance on sinoatrial (SA) rate and antegrade atrioventricular (AV) conduction. The arterial pressure stimulus for these reflexes was produced by intra-aortic balloon inflation (increase) and hemorrhage (decrease); the efferent sympathetic reflex was blocked by spinal cord transection. The dromotropic response to arterial pressure changes was studied over a physiological range of arterial pressures (60-150 mmHg) with the chronotropic response intact, with atrial pacing to prevent the chronotropic response, and after atropine or bilateral vagotomy. In all animals, the chronotropic response to arterial pressure changes balanced the dromotropic response to preserve 1:1 AV conduction over most arterial pressures. If the chronotropic response was prevented with atrial pacing, an unbalanced and independent vagal regulation of AV conduction was "unmasked" with resultant high-grade second-degree AV block. The independent regulations of SA rate and AV conduction were further found to be finely matched to produce an equilibrium of chronotropic-dromotropic changes as arterial pressure varied. Clinical conditions arising from disruption of this equilibrium are discussed.