Case report: adenosine induced ventricular fibrillation in a patient with stable ventricular tachycardia.

Adenosine is frequently used in emergency departments and intensive care units for the termination of narrow complex tachycardias. Recently its utility in terminating wide complex tachycardias has been reported in the literature. Adenosine is generally felt to be a safe medication even though its proarrhythmic effects in the setting of narrow complex or supraventricular tachycardias have been well documented. Herein, we describe the first case to our knowledge of adenosine inducing ventricular fibrillation in a patient with a stable wide complex tachycardia that was subsequently proven to be ventricular tachycardia at electrophysiologic study.

Effects of azimilide, acidemia, and the combination on defibrillation energy requirements.

We investigated the effects of azimilide, acidemia, and the combination on the defibrillation energy requirement (DER). An anesthetized canine model of internal transvenous defibrillation with biphasic shocks was used. Dogs were assigned to receive a 0.25N HCl infusion (target pH, 7.15), azimilide, azimilide with HCl infusion, or placebo (n = 7 per treatment). DERs were determined in triplicate using an increment-decrement protocol at baseline and during each treatment. Monophasic action potentials and ECG intervals were measured at baseline and during each treatment. Analysis of variance (ANOVA) with post hoc Tukey's test was used for statistical analysis. The DER was reduced by azimilide and increased above control values by both acidemia and the combination of acidemia and azimilide. All treatment groups resulted in a significant change compared with placebo (p < 0.05). The correlation between DER and various repolarization measurements was determined. The treatment-related changes in both QT intervals and monophasic action potential (MAP) durations were inversely correlated with DER. Azimilide reduces the DER, whereas acidemia increases the DER in our model. The combination of azimilide and acidemia still resulted in an increase in the DER. This finding may have clinical implications for the use of azimilide in settings such as myocardial ischemia, in which myocardial pH is reduced.

Radiofrequency catheter ablation of atrioventricular accessory pathways in 3 dogs with subsequent resolution of tachycardia-induced cardiomyopathy.

Incessant supraventricular tachyarrhythmias are known to result in myocardial dysfunction indistinguishable from idiopathic dilated cardiomyopathy by current testing methods. This tachycardia-induced cardiomyopathy (TICM), however, is uniquely reversible with adequate rhythm control. Two dogs were presented to The Ohio State University for incessant supraventricular tachycardia (SVT) and echocardiographic signs of dilated cardiomyopathy, later proven to be TICM. A 3rd dog presented for frequent paroxysms of SVT and syncope had echocardiographic signs of mild myocardial systolic dysfunction. All 3 dogs had inadequate rhythm control with multiple antiarrhythmic agents, and 1 dog suffered from recurrent left-sided congestive heart failure. Generalized cardiomegaly was found in 1 dog and left-sided dilatation without concurrent right-sided enlargement in 1 dog. Mild-to-severe left ventricular systolic dysfunction was confirmed echocardiographically in all dogs. A total of 4 atrioventricular accessory pathways (APs) were found during invasive electrophysiologic studies in these 3 dogs. All APs were successfully ablated with radiofrequency energy delivered through a thermistor-tipped catheter. Elimination of AP conduction, and thus orthodromic atrioventricular reciprocating tachycardia, resulted in resolution of all clinical and echocardiographic evidence of TICM in these dogs. This result confirms that the cardiomyopathy was, in fact, reversible TICM. All cardiovascular medications were discontinued, and no complications occurred during a 15-25-month follow-up period.

Electrophysiologic characteristics of accessory atrioventricular connections in an inherited form of Wolff-Parkinson-White syndrome.

INTRODUCTION: A familial form of Wolff-Parkinson-White syndrome (WPW) occurs in association with hypertrophic cardiomyopathy and intraventricular conduction abnormalities. This syndrome, demonstrating autosomal dominant inheritance and segregating with a high degree of penetrance but variable expressivity, has been genetically linked to chromosome 7q3. The purpose of this study is to detail the electrophysiologic characteristics of accessory atrioventricular connections (AC) in four members of a kindred with this syndrome. METHODS AND RESULTS: We clinically evaluated 32 members of a single kindred and identified 20 individuals with ventricular preexcitation, abnormal intraventricular conduction including complete AV block and/or ventricular hypertrophy. Genetic linkage analysis mapped the disease gene in this kindred to the chromosome 7q3 locus (maximum logarithm of the odds score = 6.88, theta = 0); recombination events in affected individuals reduced the genetic interval from 7 centimorgans (cM) to 5 cM. Electrophysiologic study of four individuals with preexcitation, identified seven AC (1 right sided, 3 septal, and 3 left sided). All four individuals had inducible orthodromic tachycardia; while three had multiple AC. Bidirectional conduction was demonstrated in 6 of 7 AC. Successful ablation was accomplished in 5 of 7 AC. CONCLUSION: The electrophysiologic characteristics and location of AC in family members having this complex cardiac phenotype are similar to those seen in individuals with isolated WPW. Identification of WPW in more than one family member should prompt clinical evaluation of relatives for additional findings of ventricular hypertrophy or conduction abnormalities.

Preliminary clinical results of a biphasic waveform and an RV lead system.

Biphasic defibrillation waveforms have provided a reduction in defibrillation thresholds in transvenous ICD systems. Although a variety of biphasic waveforms have been tested, the optimal pulse durations and tilts have yet to be identified. A multicenter clinical study was conducted to evaluate the performance of a new ICD biphasic waveform and new RV active fixation steroid eluting lead system. Fifty-three patients were entered into the study. Mean age was 63 years with a mean ejection fraction of 36.8%. Primary indication for implantation was monomorphic ventricular tachycardia alone (54.7%). Forty-eight patients (90.6%) were implanted with an RV shocking lead and active can alone as the anodal contact. The ICD can was the cathode. In four cases (7.5%), an additional SVC or CS lead was used due to a high DFT with the RV lead alone. In an additional case, a chronic SVC lead was used although the RV-Can DFT was acceptable. DFT for all cases at implant was 9.8 +/- 3.7 J. Repeat testing at 3 months for a subset of patients showed a reduction in DFT (7.4 +/- 3.0 J), P value = 0.03. Sensing and pacing characteristics of the RV lead system remained excellent during the study period (acute 0.047 +/- 0.005 ms at 5.4 V and 9.9 +/- 6.2 mV R wave; chronic 0.067 +/- 0.11 ms at 5.4 V and 9.3 +/- 5.4 mV R wave). It is concluded that this lead system provides good acute and chronic sensing and pacing characteristics with good DFT values in combination with this waveform.

Implantable defibrillators impedance measurement using pacing pulses versus shock delivery with intact and modified high voltage lead system.

At present the only method for measuring the high voltage system lead impedance in patients with an ICD is to deliver a low energy test shock. This is painful, requires sedation, and carries a risk of ventricular fibrillation induction. We sought to assess the shock lead and electrode function by calculating IMP using low voltage pacing pulses, and compared it to the measured impedance of a shock through the same lead. This was performed in both an intact and a modified lead system in order to mimic common clinical scenarios that alter lead system IMP (e.g., lead fracture). In an anesthesized canine model (n = 12) a standard (S) transvenous defibrillation lead (TDL), a modified (M) TDL (two-thirds of coil covered with heat-shrunk tubing), an active can (AC), and a M epicardial patch (EP) (two of four coils were disconnected) were used. Three configurations (C) were tested: C1:S/TDL-->AC, C2:M/TDL-->AC, and C3:M/TDL-->MEP. A measured IMP was obtained by an ICD using a 5-J shock as control. IMP was calculated using a 5-J shock, pacing pulses of 10-, 5-, 2-, and 1-V amplitude, as well as from a square wave drive train of low amplitude/high frequency signals (1 and 0.2 V, at 10 kHz) in all Cs. Ohm's law (V = IR) was utilized for measuring calculated IMP. As the surface area of the high voltage lead system decreased, the mean measured IMP (control) increased from C 1 to 3 (63 +/- 10, 95 +/- 4, and 127 +/- 20 omega, respectively). The correlation of calculated IMP from all Cs to measured impedance (control) remained high throughout the IMP range (range of correlation coefficient (r): 0.921-0.981). Calculated IMP using delivery of pacing pulses is highly correlated to IMP measured during shock delivery. This correlation remains high over a clinically significant range of high voltage lead system IMP changes. This study suggests that pacing pulses can be used to predict the IMP changes in the high voltage lead system which may occur clinically, reducing the need to deliver a shock for IMP measurement.

The influence of specific and nonspecific potassium current blockade on the defibrillation energy requirement of biphasic shock.

UNLABELLED: Block of delayed rectifier potassium current (IK) is known to decrease defibrillation energy requirements (DERs). We tested the hypothesis that there would be no difference in DER reduction with a nonspecific IK (IKr + IKs) blocker, ambasilide, and a specific IKr blocker, dofetilide. METHODS: An anesthetized canine model (n = 30) of internal transvenous defibrillation with biphasic shocks was used. Ambasilide (n = 9; dose: 4.8 mg/kg, then 9.6 mg/kg/hour), dofetilide (n = 10; dose: 10 (micrograms/kg, then 3.6 (micrograms/kg/hour), or matched placebo (n = 11) were administered. DERs (J) were determined in triplicate using an increment-decrement protocol at baseline and during each treatment. ECG intervals were measured at baseline and during each treatment. ANOVA with post-hoc Bonferroni test was used for statistical analysis. RESULTS: Ambasilide resulted in a +23.5 +/- 4.06% prolongation of the QTc interval, while dofetilide resulted in a +20.5% +/- 3.76% prolongation of the QTc interval. Thus, the two drugs resulted in comparable prolongation of the QTc interval (P < 0.05 compared to placebo). Both drugs significantly reduced the DER (-17.7% +/- 5.33% reduction by ambasilide, and -21.9% +/- 5.21% reduction by dofetilide, P < 0.05 compared to placebo). There was no difference in the magnitude of DER reduction between the two treatments. CONCLUSIONS: Administration of equipotent doses (as indicated by QTc changes) of ambasilide or dofetilide had comparable effects on DERs. Selectivity of IK blockade has no significant effect on the magnitude of reduction in DERs.

Improved clinical efficacy of external cardioversion by fluoroscopic electrode positioning and comparison to internal cardioversion in patients with atrial fibrillation.

BACKGROUND: Despite using different electrode positions, "conventional" external DC cardioversion in patients with atrial fibrillation is ineffective in 6%-50% of cases. An alternative when DC cardioversion is not successful is low energy internal cardioversion, which is performed at increased risk. We tested the hypothesis that optimization of electrode pad position under fluoroscopy to encompass as much atrial muscle as possible might improve the success rate of external cardioversion and thus minimize the need for internal cardioversion. METHODS: Fifteen (9 males, 6 females) patients (age: 54 +/- 15 years, weight: 124 +/- 35 kg) with chronic atrial fibrillation (> 8 weeks) who had undergone unsuccessful conventional external cardioversion entered the study. Repeat conventional external cardioversion with electrodes in standard (right anterior and left posterior) positions was followed by "optimized" external cardioversion by positioning electrodes under fluoroscopy (using metallic markers). In case of failure, internal cardioversion was performed. RESULTS: All 15 patients had undergone unsuccessful conventional external cardioversion with 360-J shocks. Eight patients (group A) reverted to sinus rhythm with one or two 360-J shocks using fluoroscopy-guided pad placement (53%). Six of the remaining 7 (86%) patients (group B) had successful internal cardioversion with biphasic shocks (12 +/- 3 J). The body weight and body mass index were statistically lower in group A vs group B (106 +/- 27 vs 145 +/- 33 kg, p = 0.03 and 35 +/- 8 vs 45 +/- 8 kg/m2, P = 0.48, respectively). There was no statistically significant in age, height, body surface area, duration of atrial fibrillation, amiodarone therapy, ejection fraction, or underlying heart disease. CONCLUSION: Unsuccessful external DC cardioversion, in some patients, is in part due to suboptimal conventional positioning of electrode pads that can be improved under fluoroscopic guidance by achieving the best possible vector encompassing the right and left atria. The optimized external cardioversion technique may minimize the need for internal cardioversion, which remains an effective approach when external cardioversion fails.

Clinical characteristics of sudden death victims in heritable (chromosome 1p1-1q1) conduction and myocardial disease.

OBJECTIVES: The purpose of this study was to identify the clinical characteristics of family members at risk of sudden death. BACKGROUND: The significance of sudden death in heritable cardiac disorders with delayed expression is incompletely understood. Additional insights come from a four-decade experience of seven generations of a family of German origin with autosomal dominant (chromosome 1p1-1q1) cardiac conduction and myocardial disease. METHODS AND RESULTS: A total of 38 family members (20 males; 18 females) were identified with sudden death. Twenty-eight family members (mean age 48+/-8 years) from earlier generations had no pacemaker at the time of sudden death. In this group, 15 subjects were asymptomatic prior to sudden death. Ten family members with sudden death, from later generations, had chronically implanted pacemakers for high grade atrioventricular block. This group was older (mean age 57+/-2 years), with decreased functional status (New York Heart Association class II to IV), enlarged left atria, dilated left ventricles with reduced systolic function and documented ventricular fibrillation in three members. Twenty-eight family members with sudden death were descendants of sib lineages 2 or 6; 21 family members with sudden death were offspring of a parent who also suffered sudden death. CONCLUSION: Sudden death is an important late outcome in heritable (chromosome 1p1-1q1) cardiac conduction and myocardial disease. Pacemaker therapy is important for the treatment of symptomatic bradycardia, but it does not prevent sudden death. Family members who are beyond the third decade of life with reduced functional capacity, left ventricular dysfunction, pacemakers and who are the offspring of a parent with sudden death appear to be at greatest risk

QRS duration widening: reduced synchronization of endocardial activation or transseptal conduction time?

Antegrade activation of the His-Purkinje system (HPS) results in synchronized activation of the right ventricular (RV) and left ventricular (LV) endocardia forming normal, narrow QRS duration (QRSD). An alteration in septal activation and transseptal conduction time have been reported to be the causes for QRSD widening seen with bundle branch block. However, reduced synchronization of activation of RV and LV endocardia as another potential mechanism for QRSD widening has not been systematically studied. Fifteen consecutive patients underwent radiofrequency ablation (RFA) for treatment of supraventricular tachycardia. After RFA, mean QRSD in normal sinus rhythm was 86 +/- 8 ms with mean HV interval of 40 +/- 5 ms. Right atrial (RA), coronary sinus (CS), simultaneous (S) RA-CS, RV apex (RVA), LV apex (LVA), and SRVA-LVA pacing were performed. Mean QRSD with RA, CS, SRA-CS pacing was similar to normal sinus rhythm (87 +/- 7, 87 +/- 8 and 88 +/- 8 ms respectively). Mean QRSD was significantly longer with SRVA-LVA and either RVA or LVA pacing alone compared to normal sinus rhythm (106 +/- 8, 146 +/- 12 and 157 +/- 13 ms, respectively). However, QRSD was significantly shorter with SRVA-LVA pacing compared to either RVA or LVA pacing alone (P < 0.0001). We conclude that shorter QRSD with SRVA-LVA pacing compared to either RVA or LVA pacing alone is due to elimination of transseptal conduction delay; longer QRSD with SRVA-LVA pacing compared to sinus or atrial paced rhythm is due to reduced synchronization of endocardial activation secondary to ectopic entry of impulses into the HPS network and inability to take advantage of the branching structure of the HPS. Therefore, in addition to transseptal conduction delay, reduced synchronization of endocardial activation is another potential mechanism for QRSD widening.

Drug and defibrillator interactions.

We reviewed the interactions of drugs and defibrillators, with emphasis on implantable cardioverter defibrillators. Articles were identified by searching MEDLINE from 1966 to the present; additional sources were identified from reference lists in these articles. Drugs have the potential for both beneficial and harmful interactions with electrical therapy. Beneficial interactions include reductions in the energy required to defibrillate the heart and in the occurrence of arrhythmia resulting in decreased shock frequency, prolonged device longevity, and improved patient comfort. Potentially harmful interactions include altering the detection of ventricular tachycardia; altering the pacing threshold, resulting in interference with bradycardia or antitachycardia pacing; development of incessant ventricular tachycardia; and increasing the energy required to defibrillate the heart. As the use of implantable cardioverter defibrillators increases, pharmacists should be aware of the potential for drug-device interactions.

Interrelations between QRS morphology, duration, and HV interval changes following right bundle branch radiofrequency catheter ablation.

Interrelations between QRS morphology, duration, and HV interval changes in a model of "complete" bundle branch block following right bundle branch radiofrequency ablation have not been subjected to systematic study. This article describes these interrelations in patients who underwent right bundle ablation. Over a period of 42 months, 16 patients underwent radiofrequency ablation of the right bundle for treatment of bundle branch reentrant tachycardia. All 16 patients had prolonged HV interval at baseline (minimum = 60 ms; mean = 68 +/- 8 ms). After ablation, one patient developed complete heart block; the remaining 15 patients developed complete right bundle branch block (RBBB) and further prolongation of the HV interval (increment = 24 +/- 16 ms). In 14 of these 15 patients, QRS duration was 138 +/- 26 ms before ablation and increased to 168 +/- 13 ms after ablation. In the remaining patient, the QRS duration was 160 ms before ablation and shortened to 144 ms following ablation despite further HV prolongation. Larger increases of HV interval after ablation were associated with smaller or negative changes in QRS duration (r = -0.77). Three was a direct relationship between QRS duration at baseline and the increment in HV interval after ablation (r = 0.70), and an inverse relationship between QRS duration before and after ablation (r = 0.84). Radiofrequency ablation of right bundle may be associated with an increase in HV interval and QRS duration. However, HV interval prolongation is not necessarily associated with QRS duration widening. A large change in HV interval is more likely to be associated with an already prolonged QRS duration before ablation and a lesser increase or even decrease in QRS duration after ablation. A shorter QRS duration before ablation is associated with a smaller HV interval increase following ablation but a greater increment in QRS duration. These findings are consistent with the concept that narrowness of QRS duration is due to synchronized activation of ventricular endocardium; whereas, QRS duration widening seen with His-Purkinje damage is due to reduced synchronization of endocardial activation.

Clinical significance of an equivocal signal-averaged electrocardiogram.

Patients with an equivocal signal averaged electrocardiogram (SAECG) had less heart disease and better prognosis than patients with overtly abnormal SAECGs. An equivocal SAECG should not prompt further invasive diagnostic testing for ventricular tachycardia unless other clinical risk factors are present.

Long-term survival and complications in patients with malignant ventricular tachyarrhythmias: treatment with a nonthoracotomy implantable cardioverter defibrillator with or without a subcutaneous patch.

The Endotak lead system and ICD has been used to treat patients with malignant ventricular arrhythmias. We analyzed the clinical characteristics of 1,053 patients who underwent implantation of the Endotak lead system with or without a subcutaneous patch. Group A consisted of 567 patients receiving the Endotak lead with a subcutaneous patch; group B consisted of 486 patients receiving the Endotak lead alone. The 2-year survivals from sudden death, cardiac death, and total death in groups A and B were 97.6%/98.2% (P = 0.38), 88.6%/92.7% (P = 0.09), and 84.7%/86.8% (P = 0.06), respectively. Minimum tested effective defibrillation energy at implantation was 17.2 +/- 5.2 J for group A and 15.8 +/- 5.1 J for group B (P < 0.01). The operative mortality was 1.8% in group A and 0.6% in group B (P = 0.09). The incidence of lead dislodgment, malfunction, and infection was 6.7% for group A and 3.5% for group B (P < 0.01). Sudden death survival was excellent in both groups with less lead complications in group B. The Endotak lead alone may be the preferred choice of lead configuration in those patients who have adequate defibrillation thresholds at implant.

Retrograde migration of the site of functional block: a mechanism underlying resolution of functional retrograde bundle branch block during AV reentrant tachycardia.

INTRODUCTION: Functional bundle branch blocks during supraventricular tachycardia have been described, and their sustainment has been attributed to concealed conduction. Such blocks frequently resolve spontaneously, but the electrophysiologic mechanism of resolution has not been well described. This report describes the resolution of functional bundle branch block through proximal migration of the site of block. METHODS AND RESULTS: During electrophysiologic study of a patient with reentrant antidromic tachycardia via an atriofascicular accessory pathway, functional retrograde right bundle branch block could be readily induced following tachycardia initiation with right ventricular apical pacing. Resolution of this block was associated with shortening of the tachycardia cycle length. Electrogram recordings along the right bundle branch during tachycardia determined that resolution of the functional retrograde right bundle branch block was associated with migration of the site of block from the distal to the proximal right bundle. When the site of block was directly at the recording site, both anterograde and retrograde activation of the right bundle was demonstrated. CONCLUSION: Migration of the site of block is a mechanism of resolution for functional conduction blocks maintained by concealed conduction.

Long-term clinical outcome of right bundle branch radiofrequency catheter ablation for treatment of bundle branch reentrant ventricular tachycardia.

The study assessed the long-term outcome of patients undergoing radiofrequency ablation of the right bundle for bundle branch reentrant ventricular tachycardia. Bundle branch reentrant tachycardia was diagnosed in 16 patients (ejection fraction 31% +/- 15%) who underwent electrophysiology study in our laboratory. All patients had His-Purkinje system conduction delay with mean HV interval of 68 +/- 8 ms. After ablation, right bundle branch block developed in 15 patients. One patient developed complete heart block, which was anticipated. One patient died of heart failure 9 months after ablation. Two patients were successfully bridged to heart transplantation 0.5 and 13 months, respectively, after ablation. Two patients received implantable defibrillators for other ventricular tachycardias. One patient had syncope 11 months after ablation, but there was no evidence of ventricular tachycardia or heart block in repeat electrophysiology study. This patient died suddenly 29 months after ablation. The remaining nine patients were alive and well for a mean follow-up of 19 +/- 10 months. Radiofrequency ablation of the right bundle branch is an effective therapy for treatment of bundle branch reentrant ventricular tachycardia. Survival is excellent provided that other types of ventricular tachycardia, when present, are treated as well. This technique may be helpful in management of patients who have unacceptable frequent shocks from their implanted defibrillators and may be helpful in avoiding implantation of such a device completely in others. In some patients with terminal heart failure and incessant ventricular tachycardia, this procedure can function as a bridge to cardiac transplantation.

Asymmetry of retrograde conduction and reentry within the His-Purkinje system: a comparative analysis of left and right ventricular stimulation.

OBJECTIVES: The purpose of this study was to delineate retrograde His-Purkinje system conduction and reentry (V3 phenomenon) during left ventricular extrastimulation and compare them with right ventricular extrastimulation. BACKGROUND: The V3 phenomenon has been well described in the past during right ventricular extrastimulation; however, it has not been studied systematically during left ventricular extrastimulation. METHODS: Left and right ventricular pacing were performed in 13 patients. Retrograde and anterograde routes of impulse propagation were determined on the basis of the sequence of His (H) and right bundle (RB) potentials, H-RB intervals, as well as the QRS configuration and axis of V3 beats. RESULTS: During right ventricular pacing, retrograde conduction of V2, when discernible, occurred exclusively through the left bundle at all coupling intervals equal to or shorter than the His-Purkinje relative refractory period, with the exception of two isolated beats. During left ventricular extrastimulation, His bundle activation was through the left bundle in nine patients and through the right or left bundle in three other patients. In one patient, the route could not be determined. The V3 phenomena occurred in eight patients during right ventricular pacing. Seven patients had a left bundle branch block pattern QRS configuration, and one had a right bundle branch block pattern configuration. V3 beats occurred in five patients during left ventricular apex pacing: left bundle branch block pattern configuration in one patient and right bundle branch block pattern configuration in four. In three of these four patients, the reentry was interfascicular and limited to the left bundle branch system. CONCLUSIONS: The left-sided His-Purkinje system is the preferred retrograde route of impulse propagation during both left and right ventricular extrastimulation. Reentry within the His-Purkinje system elicited by right ventricular extrastimulation involves both bundle branches, whereas this reentry tends to occur within the left-sided His-Purkinje system during left ventricular pacing.

Evaluation of left ventricular function during upright exercise: correlation of exercise Doppler with postexercise two-dimensional echocardiographic results.

The relationship of regional and global left ventricular function to aortic flow dynamics during exercise was determined in 14 normal subjects and 14 patients with coronary artery disease. Doppler and two-dimensional echocardiographic studies were performed before, during, and immediately after an exercise test by the Bruce protocol. Two-dimensional echocardiography was used to determine the ejection fraction and new wall motion abnormalities. The peak ejection velocity, stroke index, and cardiac index were calculated from the pulsed Doppler tracing. In normal subjects the ejection fraction increased significantly (p less than .001) from rest (0.51 +/- 0.07) to peak exercise (0.61 +/- 0.07), while the response in coronary patients was blunted (0.49 +/- 0.11 vs 0.48 +/- 0.16). Similarly, the change in peak ejection velocity throughout exercise in normal subjects (from 0.71 +/- 0.12 to 1.50 +/- 0.35 m/sec) was significantly (p less than .01) greater than that in patients with coronary artery disease (from 0.61 +/- 0.13 to 0.90 +/- 0.29 m/sec). There was a good correlation between the percent change in peak ejection velocity and the percent change in ejection fraction from rest to peak exercise in the entire study group (rs = .64) and in the patients with coronary artery disease (rs = .84). These preliminary data suggest that exercise-induced changes in Doppler echocardiographic variables may offer a potential adjunct in the evaluation of patients with ischemic heart disease.

Effect of coronary artery disease on Doppler-derived parameters of aortic flow during upright exercise.

Recent advances in Doppler echocardiography have made possible noninvasive determination of stroke volume, cardiac output and peak ejection velocity at rest. To determine the ability of Doppler to measure these variables and the effect of altered left ventricular (LV) function during upright treadmill exercise, 20 normal subjects (group I) and 17 patients with coronary artery disease (CAD) (group II) were studied. Stroke index response was similar in both groups. The increase in cardiac index was more rapid in group I subjects and reached a higher peak value at maximal exercise (8.6 +/- 2.5 vs 5.5 +/- 2.2 liters/min, p less than 0.001). Peak ejection velocity increased rapidly during exercise in group I subjects; it increased much less in group II patients. Differences were significant at each stage of exercise. Peak ejection velocity was 1.56 +/- 0.32 and 0.89 +/- 0.26 m/s in group I vs group II patients, respectively, at maximal exercise. Three responses were seen in group II subjects. Three patients, all with 1-vessel CAD and normal LV function at rest, showed a normal response, with an increase in peak ejection velocity of at least 80% (type I response). In 8 patients peak ejection velocity increased less than 80% (type II response) and in 6 patients it decreased at maximal exercise (type III). Type II and III responses were seen in patients with more severe CAD and LV dysfunction at rest. These data show a progressive difference in Doppler-derived variables in exercise between normal subjects and patients with CAD, which is greatest in patients with LV dysfunction at rest and multivessel CAD.