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Biomedical subjects

K A Ellenbogen

Publications and source records attributed to K A Ellenbogen.

At least 127 records · Page 7Linked to original sources
PubMed1990

Changes in regional adrenergic tone during sustained ventricular tachycardia associated with coronary artery disease or idiopathic dilated cardiomyopathy.

The hemodynamic tolerance of an episode of ventricular tachycardia (VT) can vary widely from no decrease in systolic blood pressure to severe hypotension. Little is known about the factors responsible for these different responses in man. Previous animal studies have suggested an important role for vasoconstriction mediated by the alpha-adrenergic nervous system. To determine the magnitude and time course of changes in alpha-adrenergic tone during symptomatic sustained monomorphic VT, VT cycle length, mean and phasic arterial pressure, forearm blood flow (by venous occlusion plethysmography) and forearm vascular resistance were measured in 15 patients. Nine of these patients were studied before and after regional intraarterial alpha blockade with phentolamine. After the induction of VT (350 +/- 68 ms), mean forearm blood flow decreased from 3.2 +/- 1.1 to 2.2 +/- 0.8 ml/min/100 ml (p = 0.0002) and the forearm vascular resistance increased from 32 +/- 14 to 40 +/- 14 units (p = 0.01). There were no significant differences for forearm vascular resistance during the first and last 30 seconds of VT (41.3 +/- 14 vs 37 +/- 13 units). After the infusion of intraarterial phentolamine, there were no significant changes in the VT cycle length or mean arterial pressure, but the forearm vascular resistance increase during VT was blunted by 60 to 70%. Most patients with symptomatic VT demonstrate sympathetic vasoconstriction and these changes are maximal during the first 30 seconds of VT. This sympathoexcitatory response is due largely to stimulation of alpha-adrenoreceptors and may be mediated by arterial baroreflexes.

Cardiomyopathy, Dilated↗
PubMed1990

Increased vagal cardiac nerve traffic prolongs ventricular refractoriness in patients undergoing electrophysiology testing.

Stimulation of the vagus nerve in animals causes prolongation of sinus cycle length, atrioventricular nodal conduction and ventricular refractoriness. Vagal stimulation appears to have a protective effect in animal models of sudden death. The electrophysiologic effects of enhanced vagal activity on right ventricular (RV) refractoriness in man have not been studied previously. The comparative effects of enhanced vagal tone (neck suction to -60 mm Hg) on sinus cycle length and RV refractoriness were assessed in 26 patients. The electrophysiologic effects of vagal activation by stimulation of carotid baroreceptors with neck suction were compared to the effect of carotid and aortic baroreceptor stimulation with phenylephrine infusion in 12 patients. During neck suction, mean sinus cycle length (819 +/- 32 ms) was prolonged by 146 +/- 20 ms (p less than 0.0001). The mean RV effective refractory period (ERP) and functional refractory period (FRP) were prolonged by 4 +/- 1 ms and 5 +/- 1 ms (p = 0.0001 and 0.0002, respectively). The mean change in RV ERP and FRP correlated with the peak change in sinus cycle length during neck suction (r = 0.46 and r = 0.58, respectively). During intravenous phenylephrine infusion, the mean change in RV ERP and FRP was 5 +/- 2 ms (p less than 0.04) and 10 +/- 3 ms (p less than 0.01), respectively. These results show that reflex vagal stimulation with neck suction or phenylephrine infusion causes a small but significant prolongation in RV refractoriness. These findings imply that the potential benefits of enhanced vagal tone in preventing sudden death may be indirectly mediated by changes in ventricular refractoriness.

Cardiac Pacing, Artificial↗
PubMed1990

Usefulness of right ventricular pulse pressure as a potential sensor for hemodynamically unstable ventricular tachycardia.

The automatic implantable cardioverter defibrillator has had a major impact on the management of patients with ventricular tachyarrhythmias. Future devices will offer tiered therapy for ventricular arrhythmias, based on a sensor capable of discriminating hemodynamically stable from unstable ventricular tachycardia (VT). We studied 27 patients with sustained VT/ventricular fibrillation during 70 episodes of sustained ventricular arrhythmias (greater than 30 seconds or requiring cardioversion). In this study, phasic arterial pressure (mm Hg), VT cycle length (ms) and right ventricular (RV) pulse pressure (mm Hg) were measured before, during the first 30 beats and after each episode of VT. During the first 10 beats of 23 episodes of unstable VT, the mean (+/- standard error of the mean) decrease in RV pulse pressure from baseline was 22 +/- 1.8 mm Hg; it was 13.8 +/- 2.4 mm Hg during the first 10 beats of 47 episodes of stable VT, (p = 0.01, stable vs unstable). For the next 20 beats of VT, RV pulse pressure decreased from baseline by 22 +/- 2.5 mm Hg during unstable and by 12.0 +/- 2.5 mm Hg during stable VT (p = 0.0001, stable vs unstable). The percent decrease of RV pulse pressure correlated well with the percent decrease in mean arterial pressure and percent decrease in systolic arterial pressure (r = 0.70; r = 0.69, respectively; p less than 0.001) during VT, but poorly with the VT cycle length (r = 0.27, p less than 0.05). The percent decrease in RV pulse pressure is a useful hemodynamic sensor for discriminating between stable and unstable VT.

Arrhythmias, Cardiac↗
PubMed1990

New insights into pacemaker syndrome gained from hemodynamic, humoral and vascular responses during ventriculo-atrial pacing.

Ventricular pacing is performed during programmed electrical stimulation and during normal functioning of single chamber (VVI or VVIR) pacemakers. In many patients, retrograde ventriculoatrial (V-A) conduction may occur and evoke hemodynamic and reflex neurohumoral responses, which are unique to this pacing mode. Accordingly, forearm blood flow, forearm vascular resistance, mean and phasic arterial pressure, cardiac output and plasma norepinephrine, epinephrine and dopamine were measured during atrial, ventricular and V-A pacing at a cycle length of 600 ms (100 beats/min) before and after regional alpha blockade with intraarterial phentolamine in 16 patients with a left ventricular ejection fraction greater than 35% and little or no symptoms of congestive heart failure. During V-A pacing, cardiac output decreased by 10%, whereas forearm vascular resistance increased from 52 +/- 7 to 70 +/- 9 U (p less than 0.001) and plasma norepinephrine increased from 183 +/- 27 to 232 +/- 27 pg/ml (p less than 0.01). Phentolamine nearly abolished the increase in forearm vascular resistance in response to V-A pacing (18 +/- 4.1 U before vs 5.8 +/- 1.5 U after, p less than 0.05). The change in forearm vascular resistance with V-A pacing correlated with systolic arterial pressure, but not with changes in mean arterial pressure, pulse pressure, cardiac output, mean or peak right atrial pressure, pulmonary artery or pulmonary capillary wedge pressure. These results suggest that forearm vascular resistance responses to V-A pacing are mediated mainly by alpha-adrenergic receptors, through the arterial baroreflexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1990

A prospective study of right ventricular pulse pressure and dP/dt to discriminant-induced ventricular tachycardia from supraventricular and sinus tachycardia in man.

In the future, automatic implantable cardioverter defibrillators (AICD) may incorporate sensors to differentiate hemodynamically stable from unstable ventricular tachycardias (VT). These sensors should also discriminate between ventricular and supraventricular tachycardias to avoid inappropriate responses from the device. Right ventricular pulse pressure (RVPP) and maximal systolic right ventricular dP/dt (dP/dt) were measured before, during and after 91 episodes of hemodynamically stable VT (VTs), hemodynamically unstable VT (VTus), supraventricular tachycardia (SVT) and sinus tachycardia (ST) induced in 49 male patients. The mean percent changes (mean +/- S.E.M.) in RVPP from baseline (% delta RVPP) during VTs and VTus were -35 +/- 3% and -72 +/- 3%, respectively (both P less than 0.001). The % delta RVPP during ST was +56 +/- 11% (P less than 0.01) and % delta RVPP was unchanged from baseline during SVT (+2 +/- 9%; P greater than 0.01). Mean % change in RV dP/dt from baseline was -20 +/- 3% during VTs (P less than 0.001), -36 +/- 5% during VTus (P less than 0.001), +15 +/- 13% during SVT (P less than 0.01), and +85 +/- 23% during ST (P greater than 0.01). The mean percent changes in RVPP were significantly different between each arrhythmia group (P less than 0.01). The mean % changes in RV dP/dt were significantly different only between ST and VTs or VTus and between SVT and VTus. The range of values for % delta RVPP during VTs overlapped considerably with the ranges of % delta RVPP during VTus and SVT. The ranges of % delta RVPP overlapped minimally between VTus and SVT. Percent change RVPP separated each episode of VTs and VTus from those of ST. The range of common values for % delta dP/dt between all four groups was extensive. It is concluded that % delta RVPP from baseline is significantly different between groups of patients during VTs, VTus, SVT, and ST, but that a large degree of overlap in the range of values for % delta RVPP and RV dP/dt between different arrhythmias groups may limit the specificity of these hemodynamic variables in separating different arrhythmias.

Cardiac Pacing, Artificial↗
PubMed1990

The plasma catecholamine responses to ventricular pacing: implications for rate responsive pacing.

Many patients with VVI and VVIR pacemakers will alternate between periods of sinus rhythm and ventricular pacing. These rhythm shifts may be poorly tolerated by some patients. Changes in plasma catecholamine levels during these rhythm shifts may contribute to these patients' symptoms. We measured blood pressure, ejection fraction and plasma norepinephrine, epinephrine, and dopamine serially in nine patients with normal left ventricular ejection fractions and VVI pacemakers during sinus rhythm and at paced rates of 10 beats per minute (bpm) above sinus rates (10 + NSR), 100 bpm, and 130 bpm. The mean norepinephrine level at baseline was 143 +/- 16 pg/mL and increased to 166 +/- 36 pg/mL at 10 + NSR, 204 +/- 47 pg/mL at 100 bpm, and 182 +/- 34 pg/mL at 130 bpm. These increases corresponded to mean percent changes from baseline of 17% (P = 0.02), 33% (P = 0.002), and 24% (P = 0.07), respectively. The magnitude of the norepinephrine response was not correlated with the pacing rate. The mean plasma epinephrine level at baseline was 57 +/- 6 pg/mL and peaked at 51 +/- 12 pg/mL at 10 + NSR, 89 +/- 31 pg/mL at 100 bpm and 101 +/- 28 pg/mL at 130 bpm. These increases corresponded to mean percent changes from baseline of -10% (P = NS), 30% (P = 0.07), and 89% (P = 0.02), respectively. No trends in the dopamine response to pacing were noted. During ventricular pacing there were no significant changes in mean blood pressure and only slight changes in ejection fraction. The individual percent changes in plasma norepinephrine and epinephrine at 100 bpm were inversely correlated to the changes in systolic blood pressure (R = -0.68, P = 0.06, and R = -0.81, P = 0.03, respectively). These results suggest that plasma norepinephrine and epinephrine increase acutely in response to ventricular pacing at rates commonly seen during rate responsive ventricular pacing.

Aged↗
PubMed1990

Electrophysiological effects of adenosine in the transplanted human heart. Evidence of supersensitivity.

After cardiac transplantation, the denervated donor atria and ventricles demonstrate increased sensitivity to infusions of sympathomimetic amines. Recently, supersensitivity of the canine sinus and atrioventricular (AV) nodes to acetylcholine has also been demonstrated after parasympathetic denervation. Acetylcholine and the endogenous nucleoside adenosine exert similar electrophysiological effects in both the sinus and AV nodes, and share a common transduction process. We, therefore, hypothesized that after orthotopic cardiac transplantation, the donor (denervated) sinus node would demonstrate greater sensitivity to exogenous adenosine than the recipient (innervated) sinus node. The effects of incremental doses of intravenous adenosine (37-112 micrograms/kg) on changes in sinus cycle length (SCL) (delta SCLmax%), changes in PR interval (delta PRmax%), time to peak effect (sec), and duration of electrophysiological effects (sec) were prospectively measured in 28 orthotopic cardiac transplant patients and nine control subjects. The baseline SCL was 795 +/- 71 msec for the control subjects, 891 +/- 43 msec for the recipient atria, and 700 +/- 18 msec for the donor atria (p less than 0.05, donor vs. recipient). The delta SCLmax% for each dose of adenosine was similar in the innervated control and recipient atria. In contrast, the donor sinus node demonstrated a threefold to fourfold increased response to adenosine as compared with the recipient sinus node and a threefold to sixfold increased response as compared with control subjects. Similarly, the donor AV node demonstrated a threefold to fivefold increase in PR interval as compared with control subjects. The duration of sinus node slowing in the denervated atria was threefold to fivefold longer than in the recipient and control atria (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1990

Correlation of an invasive measure of right ventricular pressure and mean arterial pressure.

Recently, cardiac pacemakers have been introduced which increase heart rate during exercise. Current rate responsive pacemakers achieve this objective by monitoring minute ventilation via a transvenous impedance measurement and provides a proportional heart rate increase with increases in minute ventilation. These devices are independent of hemodynamic parameters. Therefore, the potential exists for a sufficiently high rate which results in decreased cardiac output by virtue of Starling's Principle. An invasive measure of right ventricular (RV) pressure is compatible with the power and complexity of contemporary implantable pacemakers. In addition, mean arterial pressure is accepted as a diagnostic indicator of left ventricular hemodynamic compromise. Therefore, a correlation of right ventricular pressure and mean arterial pressure was undertaken. Twenty-six patients were studied during normal sinus rhythm and ventricular tachycardia during routine electrophysiology examination. A beat to beat measure of peak to peak RV pressure resulted in a correlation coefficient of 0.68 with mean arterial pressure.

Blood Pressure↗
PubMed1989

Utility of introducing ventricular premature complexes during reciprocating tachycardia in specifying the location of left free wall accessory pathways.

The usefulness of the response to single and double ventricular premature complexes (VPCs) introduced during reciprocating tachycardia (RT) in predicting the location of a left free wall accessory pathway was studied in 55 patients with the Wolff-Parkinson-White syndrome. One VPC introduced from the right ventricle into narrow QRS RT when the His bundle was refractory resulted in retrograde atrial preexcitation in 25 of 55 (45%) patients, while 30 (55%) showed no preexcitation. Double VPCs produced retrograde atrial preexcitation in 9 of 26 patients not responding to a single VPC. No difference in RT cycle length, AH, HV or ventriculoatrial intervals was found between those patients who did or did not show retrograde atrial preexcitation. The response to single and double VPCs during RT was related to the location of the AP. The average distance of the AP from the crux determined by intraoperative epicardial mapping in the 41 patients who underwent surgery was 2.7 +/- 0.7 mapping units (left posterolateral region) in patients showing retrograde atrial preexcitation with a single VPC, 3.6 +/- 0.7 units (at the lateral left ventricular margin) in those responding to double VPCs and 4.3 +/- 0.8 units (beyond the LV margin) in those showing no response. Left bundle--branch block (LBBB) aberrancy during RT resulted in an average 60 +/- 14 ms prolongation of the ventriculoatrial interval in 40 patients, including 5 in whom LBBB was seen only after procainamide infusion. VPCs introduced into LBBB RT resulted in significant retrograde atrial preexcitation in 6 additional patients in whom no response during normal QRS RT was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Bundle-Branch Block↗
PubMed1989

Neurohumoral and hemodynamic effects of lower body negative pressure in patients with congestive heart failure.

Baroreflex modulation of forearm vascular resistance (FVR) has been reported to be abnormal in patients with congestive heart failure (CHF). However, the neurohumoral mechanisms for this impairment are not defined. We assessed the responses of arterial pressure, FVR, plasma norepinephrine, and plasma renin activity to lower body negative pressure in 29 patients with compensated CHF (New York Heart Association class III and IV) and in 11 normal age-matched control subjects. Baseline mean arterial pressure (83 +/- 2 vs 84 +/- 2 mm Hg) and mean arterial pressure during LBNP (-10, -20, and -40 mm Hg) were not significantly different in the two groups. Basal FVR (43.7 +/- 4 vs 27 +/- 2 units), plasma norepinephrine (605 +/- 81 vs 155 +/- 8 pg/ml), and plasma renin activity (8.3 +/- 1.7 vs 1.2 +/- 0.2 ng/ml/hr) were significantly (p less than 0.01) higher in patients with CHF. The relative increases in FVR responses during LBNP of -10, -20, and -40 mm Hg (10 +/- 4% vs 70 +/- 12%, 17 +/- 6% vs 106 +/- 21%, and 24 +/- 9% vs 152 +/- 28%) were markedly attenuated in patients with CHF compared to control subjects. Plasma norepinephrine and plasma renin activity responses during LBNP were also attenuated in patients with heart failure. Our results suggest that baroreflex control of FVR and plasma norepinephrine and plasma renin activity is impaired in CHF because of the inability of the cardiopulmonary baroreceptors to alter sympathetic outflow.

Adult↗
PubMed1989

Subnormal heart period variability in heart failure: effect of cardiac transplantation.

Heart period variability and arterial baroreceptor-cardiac reflex function were studied in cardiac transplant patients to determine if correction of heart failure restores parasympathetic control mechanisms toward normal. Heart period variability (standard deviation [SD] of 120 consecutive RR or PP intervals) was measured at supine rest in 34 patients with congestive heart failure (23 patients receiving diuretics, digoxin or vasodilators and 11 patients weaned from all medications), 30 cardiac transplant patients (both innervated recipient and denervated donor atrial rates) and 16 age-matched healthy control subjects. Arterial baroreflex gain was evaluated with intravenous bolus injections of phenylephrine in 22 transplant patients. Mean heart period variability (+/- SEM) was significantly lower (p less than 0.05) in the heart failure groups (22 +/- 3 ms for medicated and 17 +/- 3 ms for nonmedicated) than in the transplant patients (41 +/- 5 ms) or control subjects (58 +/- 5 ms). Heart period variability of the transplant patients was less than that of the control patients (p less than 0.05). A stepwise regression model revealed that heart period variability was inversely related to systolic arterial pressure and directly related to time after transplantation (R2 = 0.39; p = 0.03) in the transplant patients. Baroreflex gain of normotensive transplant patients was normal (11.7 +/- 1.0 ms/mm Hg) and correlated directly with heart period variability (r = 0.62; p less than 0.001). These data suggest that subnormal levels of cardiac parasympathetic activity at rest associated with congestive heart failure can be restored progressively toward normal by correction of congestive heart failure after cardiac transplantation. Post-transplant hypertension opposes this correction of baseline parasympathetic activity.

Adult↗
PubMed1989

Pharmacological characterization of conduction over a Mahaim fiber: evidence for adenosine sensitive conduction.

The presence of a nodoventricular pathway (Mahaim fiber) has been invoked to explain certain distinctive electrocardiographic and electrophysiological observations. The presence of an atrioventricular or atriofascicular fiber with decremental conduction properties has been documented in many of these patients. We report the case of a patient with a Mahaim fiber and the response to conduction over this pathway after adenosine, procainamide, encainide, verapamil, edrophonium, phenylephrine and isoproterenol. Conduction over the Mahaim fiber was blocked by adenosine, but not verapamil. The time course of adenosine induced block over the Mahaim fiber differed from adenosine induced AV nodal block. Mahaim fibers are decrementally conducting pathways that are adenosine sensitive. These findings support the concept that conduction in accessory pathways manifesting decremental properties is not mediated by the calcium channel.

Adenosine↗
PubMed1989

Pericardial repair of endocardial defect following regional endocardial resection for ventricular tachycardia.

Regional endocardial resection is the accepted surgical treatment for sustained monomorphic ventricular tachycardia. In patients requiring extensive endocardial resection, or with large aneurysms involving the interventricular septum, the resulting defect may result in weakened myocardium and, ultimately, ventricular septal defect or ventricular rupture. A new approach for repair of the resulting defect is proposed using an autogenous pericardial patch sutured to normal endocardium and included in the aneurysm repair. This technique was performed in six patients undergoing surgery for drug refractory ventricular tachycardia. All patients had large anterior left ventricular aneurysms with endocardial scar extending onto the septum. The large endocardial defect left after endocardial resection and aneurysmectomy was repaired with a pericardial patch. No intraoperative complications (e.g., suture line bleeding) were observed as a result of this technique. All patients are alive, and five of the six patients no longer have inducible ventricular tachycardia. An improvement in congestive heart failure symptoms at 1-9 months of follow-up was noted following surgery. We conclude that the pericardium can be safely used to cover endocardial defects resulting from regional endocardial resection for sustained ventricular tachycardia.

Animals↗
PubMed1989

Arterial baroreflex abnormalities in heart failure. Reversal after orthotopic cardiac transplantation.

Arterial baroreflex control of the heart and peripheral circulation is markedly impaired in humans and animals with congestive heart failure. After reversal of heart failure in animal models, arterial baroreflex control of heart rate remains impaired for up to 8 months. Cardiac transplantation restores normal ventricular function and completely reverses heart failure, but does it normalize arterial baroreflex control of heart rate in humans? We studied baroreflex sensitivity in 11 patients with severe heart failure, six normal control patients, and 23 patients at 2 weeks to 4 years after orthotopic cardiac transplantation. Baroreflex sensitivity was assessed with intravenous bolus injections of phenylephrine and is expressed as change in RR or PP interval (msec) per millimeters of mercury rise in systolic arterial pressure. Atrial rate of both donor (denervated) and recipient (innervated) atria were measured in the transplant group. Baroreflex sensitivity in patients with severe heart failure was 2.0 +/- 0.3 msec/mm Hg, but in patients after cardiac transplantation, it was 13.0 +/- 0.9 msec/mm Hg (p less than 0.001). The responses in the transplant group were similar to those observed in normal controls (10 +/- 1.2 msec/mm Hg, p = NS). Our data indicate that patients with severe congestive heart failure have marked abnormalities of baroreflex control, which are reversed as early as 2 weeks after cardiac transplantation. In view of this rapid reversal, we consider it unlikely that abnormal baroreflex sensitivity seen in heart failure is due to structural alterations in the baroreceptors. We speculate that neurohumoral rather than structural abnormalities account for depressed baroreflex sensitivity in heart failure.

Adult↗
PubMed1989

Bradyarrhythmias, emergency pacing, and implantable defibrillation devices.

This article reviews new developments in the field of cardiac pacing. Special emphasis is placed on dual chamber temporary pacing, external transthoracic cardiac pacing, and antitachycardia pacing. The role of the automatic implantable cardioverter defibrillator (AICD) in patients with sudden cardiac death is also explored with emphasis on the presentation of such patients to intensive care units.

Bradycardia↗