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Internal mammary artery (IMA) angiography can be difficult and time-consuming. We evaluated a custom designed balloon-tipped catheter, a Berman catheter (Arrow International, Reading, PA) modified by creating an end-hole to allow passage of a wire through the central lumen, for imaging the IMA without selective cannulation. We compared ease of use, procedure time, and image quality of the new catheter with the standard selective catheter technique. Thirty-six patients with IMA grafts were randomly assigned to imaging with either the study catheter or a standard catheter. Image quality, graded from poor to excellent, time to catheter placement in the subclavian artery (TIME 1), time to initial IMA angiography (TIME 2), and the difference between these two (TIME 3) were recorded. TIME 3 defined the time required to find and seat the catheter at the IMA site. The image quality was good or excellent in all but one patient. This one patient, randomized to the standard catheter technique, had poor image quality with the selective catheter. However, exchange for the study catheter resulted in excellent image quality. There was no difference in TIME 1 (P = 0.57) or TIME 2 (P = 0.55) between the two techniques. There was a significant difference in TIME 3 (P = 0.05) favoring the study catheter. There were no complication using either technique and the total contrast volume used was not significantly different between the two techniques (P = 0.32). We conclude that a new catheter technique for imaging the IMA without selective cannulation is safe, fast, easy to use, and may offer particular advantage in patients whose internal mammary artery is difficult to access.

Signal averaging has been performed to evaluate late potentials following infarction and the administration of thrombolytic therapy. Most studies have recorded signal-averaged electrocardiograms (SAECGs) at least 12 hours after the onset of the infarction. In this study, SAECGs were recorded before thrombolytic therapy and serially over 7-10 days following infarction in 21 patients. The high frequency QRS duration was significantly shortened at 1 and 24 hours compared to presentation (96.8 +/- 11.3 ms and 93.4 +/- 8.0 ms vs 103.3 +/- 14.3 ms, respectively, P < 0.05) and there was an increase in the terminal voltage over time, significant at 1 hour and 3 days (57.3 +/- 29.1 microV and 58.6 +/- 44.7 microV vs 44.4 +/- 35.5 microV, respectively, P < 0.01). Five patients met criteria for ventricular late potentials on at least one SAECG. The prevalence of late potentials was higher in patients with Q wave infarctions, or with occluded infarct related arteries. These changes in myocardial activation may be related to ischemia and reperfusion, and may not correlate with the development of a fixed substrate for reentry.

Signal averaging can be used to assess changes in myocardial activation under a variety of physiological conditions including stress. This study prospectively evaluated patients who underwent rest and exercise recording of signal-averaged electrocardiograms. The 163 patients were divided into three groups based on thallium results: normal (group I), reperfusion (group II), and fixed defect (group III). Patients in group I showed shortening of the high frequency duration (P = 0.02) and the duration of the low amplitude signal (P = 0.024) after exercise. In these patients the terminal root mean square amplitude (RMSA) also increased significantly (P = 0.005). However, patients who were in either group II or group III showed little change in signal averaging measurements after exercise. The amplitude of the QRS in V5 and the RMSA of the total QRS also increased in all groups following exercise, with a lesser increase in the patients with reperfusion by thallium imaging (group II). There was no change among groups in the incidence of ventricular late potentials with exercise. This suggests that patients with ischemia or infarction may not have the same response to an increase in sympathetic tone with exercise as patients without abnormalities of cardiac perfusion. The clinical implications of these findings may include demonstration that an area of slow conduction exists in these latter two groups of patients.

Rationale and Objectives: The authors compared complications and hemodynamic and electrophysiologic effects of two formulations of diatrizoate, one with additives that bind calcium and one without, in diagnostic cardiac angiography., Methods: Two hundred twenty-three consecutive low-risk patients alternately received Hypaque 76 (group 1, little calcium binding effect), and MD 76 (group 2, significant calcium binding). Electrocardiographic and hemodynamic changes related to coronary angiography and left ventriculography were measured, and complications requiring treatment were recorded., Results: There were more complications in patients in group 2 than in group 1 (18 versus 8, P = 0.04). Arterial pressure fell more, the QT interval increased more, and the heart rate fell more in group 2 after coronary angiography., Conclusions: Formulations of diatrizoate that minimize calcium binding are advocated for cardiac angiography when using high osmolality contrast media. The more detrimental effects that calcium binding has on myocardial function and cardiac conduction may lead to the higher incidence of complications.

Background: We surveyed patient attitudes about driving and about driving restrictions for patients with automatic defibrillators and pacemakers, and we assessed risk of arrhythmias occurring during driving., Methods: One hundred two patients responded to a questionnaire (57 patients with defibrillators and 45 patients with pacemakers) about driving habits and opinions on restriction of patients who have devices and want to drive. In addition, the literature was reviewed for approximate incidences of sudden death and syncopal or nonsyncopal device therapy to estimate risk while driving of having a defibrillator discharge., Results: Thirty-two patients with defibrillators (56%) and 28 patients with pacemakers (62%) currently drove an average of 196 and 161 km/wk, respectively. Most patients felt that driving was a right and 75% felt that restriction imposed a hardship on them. Respondents felt that common sense, limited distances, or physician input should set driving limitations. A minority felt that no restrictions should be placed on these drivers or that they should not drive at all. The risks of sudden death and syncopal and nonsyncopal defibrillator discharge were estimated at 0.0009%, 0.0011%, and 0.0015% per kilometer driven, respectively, based on weekly kilometers and published occurrences of these phenomena., Conclusions: Patients perceive that driving is their right and that there is a low risk of an arrhythmic event behind the wheel. The estimated risk and published accounts of sudden death support this. However, concurrent medical problems and stresses imposed by driving may increase risk. The physician must make reasonable recommendations to ensure patient and public safety, keeping in mind both state and federal driving regulations and reporting requirements.

To evaluate the efficacy and safety of oral amiodarone in the treatment of recurrent, sustained, refractory ventricular arrhythmias, rapid high-dose oral loading was used to treat 12 critically ill patients with frequent, sometimes incessant, sustained ventricular arrhythmias refractory to 2 to 6 antiarrhythmic agents. Presenting arrhythmias included sustained monomorphic ventricular tachycardia and ventricular fibrillation associated with cardiac arrests in 6 patients. Patients experienced 2 to 10 episodes (mean 5 +/- 2) of sustained ventricular arrhythmias over a mean period of 6.2 +/- 5.0 days (range 1 to 14) before oral amiodarone was initiated at 1,200 to 1,400 mg/day. This included at least 1 to 4 episodes (mean 2.2 +/- 1.1) within 24 hours before amiodarone. One to 4 antiarrhythmic drugs were administered concurrently during amiodarone loading. Sustained ventricular arrhythmias no longer occurred after a mean of 5.2 days (range 1 to 22) with amiodarone. Arrhythmias were controlled in 4 patients within 24 hours, 5 patients within 48 hours, 7 patients within 4 days and 10 patients within 6 days. Patients experienced a mean of 0.6 +/- 0.8 episodes within 24 hours after amiodarone. Nine patients survived to hospital discharge. No patient had significant adverse effects during high-dose loading. In conclusion, high-dose oral amiodarone loading, when added to previously unsuccessful conventional antiarrhythmic therapy, is safe and often rapidly effective for at least short-term control of frequent, refractory, sustained ventricular arrhythmias.

Cardiac tamponade, a potentially lethal complication following cardiac surgery, may present either early or late postoperatively and may be difficult to diagnose due to atypical clinical, hemodynamic, or echocardiographic findings. To determine the frequency and clinical features of postoperative cardiac tamponade, we performed a review of 510 consecutive patients who underwent cardiac surgery. The incidence of postoperative cardiac tamponade was 2.0 percent (10/510 patients) and occurred following valvular, bypass, and aortic surgery. Nine of ten patients had either atypical clinical, hemodynamic, and/or echocardiographic findings. The diagnosis of tamponade was made 1 to 30 days (mean = 8.5 days) postoperatively. Presenting symptoms were often mild and nonspecific. Classic signs including hypotension, pulsus paradoxus greater than 12 mm Hg, and elevated jugular venous pressure were present in 7, 6, and 5 patients, respectively. Right heart hemodynamics revealed elevated and equalized diastolic pressures in three of six patients. Two-dimensional echocardiography revealed selective compression of the left ventricle (LV) (four patients), right ventricle (RV) (one patient), left atrium (LA)/RV (one patient), LA/LV (one patient), LA/LV/RV (one patient), all four chambers (one patient), and no diastolic collapse of any chamber (one patient). There was often an absence of anterior pericardial fluid (six patients) with tethering of a portion of the RV to the chest wall anteriorly (five patients). Coagulation parameters were "supratherapeutic" in only three of eight patients who were receiving systemic anticoagulants at the time of diagnosis. The initial diagnosis was confused with congestive heart failure in one patient, pulmonary embolism in three patients, acute myocardial infarction in two patients, and sepsis in one patient. Eight of ten patients survived; all of these patients underwent surgical removal of fluid and/or hematoma in the operating room. We conclude that postoperative tamponade after cardiac surgery may have varied clinical and hemodynamic presentations, often due to selective chamber compression by loculated fluid or clot. Due to its frequently atypical features and presentation that may simulate other disorders, the diagnosis of tamponade should be considered whenever hemodynamic deterioration or signs of low output failure occur in the postcardiotomy patient.

The pharmacokinetics, antiarrhythmic activity and safety of intravenously administered recainam were evaluated in 15 men and 3 women. All patients had frequent (> 30/hour) ventricular premature complexes (VPCs) and unsustained ventricular tachycardia. Recainam was administered at a loading dose of 4.5 mg/kg/hour over 40 minutes, followed by a maintenance infusion of 0.9 mg/kg/hour for 23 hours and 20 minutes. Sixteen patients had satisfactory efficacy data. The mean frequency of total VPCs decreased by 92.6% and the mean frequency of runs decreased by 99.9% during the maintenance infusion. Suppressions of > or = 70% of total VPCs and > or = 90% of runs were maintained over the 23-hour, 20-minute maintenance infusion period in 16 of the 18 patients. During the maintenance infusion, hourly group plasma recainam concentrations ranged from mean +/- SD 2.6 +/- 0.7 to 3.4 +/- 0.9 micrograms/ml. Patients were observed for 24 hours after termination of the infusion. Periodic blood samples were obtained during and after termination of the infusion to determine recainam concentration. Urine specimens were collected over scheduled intervals to determine urinary excretion of recainam. A 2-compartment pharmacokinetic model was used to analyze the data. The following pharmacokinetic parameters were obtained: terminal elimination half-life, 5.0 +/- 0.8 hours; systemic clearance, 0.27 +/- 0.08 liter/hour/kg; and central and steady-state volume of distribution, 0.32 +/- 0.11 and 1.4 +/- 0.4 liter/kg, respectively. Adverse experiences were reported in 4 of the 18 patients, possibly drug-related in 2; none was considered severe or required discontinuation of recainam.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of patients with syncope often includes a battery of noninvasive tests. In this study, 45 patients (26 with suspected neurologic and 19 with suspected cardiac syncope) were evaluated with simultaneous 24-hour electroencephalographic (EEG) and 2-channel electrocardiographic (ECG) recordings. Isolated cardiac rhythm abnormalities were noted in 21 patients, but none of these was symptomatic and no definitive arrhythmias occurred. Isolated EEG abnormalities were noted in 11 patients, 5 of whom had EEG abnormalities consistent with seizure disorders. Simultaneous EEG and ECG abnormalities were seen in 4 patients. In 2 cases, a previously unsuspected etiology for syncope was found: seizures in 1 patient with heart disease, and sinus pauses in another thought to have a seizure disorder. Thus, combined ambulatory EEG/ECG monitoring may prove useful in the evaluation of some patients with syncope.

Understanding spontaneous fluctuations in ventricular tachycardia cycle length is required to develop algorithms for ventricular tachycardia detection and termination. Variations in cycle length, time to stable cycle length and the range of RR intervals during ventricular tachycardia were analyzed in 74 episodes of sustained monomorphic ventricular tachycardia induced in patients not taking antiarrhythmic medication. Linear regression demonstrated cycle length variability to decrease over time (41 +/- 24 to 17 +/- 19 ms, p less than 0.001). Slower ventricular tachycardia had more cycle length variability than faster ventricular tachycardia (p less than 0.001). Ventricular tachycardia that was initially more variable tended to remain more variable (p less than 0.001). Fifty-four percent of episodes stabilized within the first 15 beats, 75% by 30 beats and 93% by 50 beats. The number of beats to stable cycle length was independent of ventricular tachycardia rate. The average range in cycle length per episode was 127 +/- 72 ms; 12% of ventricular tachycardia episodes varied by less than 50 ms and 45% by less than 150 ms. The maximal range in RR intervals from a single episode of ventricular tachycardia was 290 ms. Therefore, ventricular tachycardia demonstrates a wide range of cycle lengths and has time-dependent changes in variability and stability. These cycle length changes should be considered in the algorithms for ventricular tachycardia detection and termination by automatic antitachycardia devices.

Antitachycardia devices currently use sustained high rate, abrupt changes in cycle length, and probability density function to determine the onset of ventricular tachycardia. Hemodynamic changes occur with the onset of tachycardia and may provide a method of discriminating supraventricular from ventricular tachycardia. In this study, patients had atrial and ventricular pressures measured during rapid atrial and ventricular pacing. Right atrial pressure increased significantly with ventricular pacing but not with atrial pacing. Right ventricular pressures did not significantly differ with atrial or ventricular pacing. The change in atrial pressure compared to baseline was greater, with ventricular pacing compared to atrial pacing. Right ventricular pressure increased compared to baseline with atrial or ventricular pacing, but there was no significant difference between pacing modalities. Measurement of right atrial pressure might prove useful in discriminating supraventricular from ventricular tachycardia.

With use of ultrafast computed tomography, 13 patients undergoing aortic valve replacement for aortic stenosis were prospectively followed to evaluate the relation between left ventricular mass and diastolic function. Studies were done before intervention, and then at 4 and 8 months later. Mass decreased from 161 +/- 11 g/m2 (+/- standard error of the mean) at baseline to 106 +/- 5 g/m2, and then to 97 +/- 7 g/m2 at 4 and 8 months, respectively, in 12 patients who demonstrated significant (greater than 20%) mass regression after operation. One patient failed to show significant changes in mass. Diastolic function, as defined by the peak filling rate of early diastole, improved (p less than 0.02) in the group with mass regression, from 2.11 +/- 0.17 s-1 at baseline to 2.12 +/- 0.23 s-1, and then to 2.62 +/- 0.26 s-1 at 4 and 8 months, respectively. Improvement in the time to peak filling rate was also noted. Heart rates were unchanged, whereas end-diastolic volumes decreased and ejection fractions increased slightly. Postoperative increase in peak filling rate correlated with regression of ventricular mass to within normal range (+/- 2 standard deviations) and attainment of New York Heart Association class I status by 8 months (p less than 0.02). Thus, improvement in diastolic function can be seen after aortic valve surgery and is associated with improved functional class. Diastolic function improves later than the regression in wall mass and may imply a delayed remodeling of the ventricle.

The clinical, angiographic and demographic characteristics of 42 patients with low-grade (less than 50%) residual stenosis at the infarct lesion after thrombolysis for acute myocardial infarction (MI) were assessed. The study group (group I) represented 21% of 198 consecutive patients receiving thrombolytic therapy over a 59-month period. Data on the 156 remaining patients were pooled for comparison (group II). Group I patients were predominantly men (86%) who were cigarette smokers (81%). Group II patients were predominantly men (75%, p greater than 0.10) but were significantly older (52 +/- 12 vs 56 +/- 10 years, p = 0.02). Prior acute MI or angina was unusual in group I. Sixty percent had no significant (greater than 50%) residual coronary artery disease while 25% had residual single artery disease. Average significant (greater than 50% diameter stenosis) residual vessel disease was 0.6 +/- 1.0 for group I and 1.9 +/- 0.9 for group II (p less than 0.001). In group I, average residual infarct lesion diameter stenosis was 36 +/- 7% in the right anterior oblique and 34 +/- 8% in the left anterior oblique views. Thirty-nine group I patients were discharged with medical therapy and 100% follow-up was obtained over a mean interval of 18 +/- 17 months. Fifteen patients experienced chest pain after acute MI accounting for 17 discrete events. Fifty-nine percent of group I had a benign course on follow-up. Eight events were classified as unstable angina, 4 as acute MI and 5 as atypical angina. Documented coronary vasospasm occurred in 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular mass and function were measured using ultrafast computed tomography, and were correlated with clinical status in 17 patients with aortic stenosis and/or insufficiency undergoing aortic valve replacement or balloon valvuloplasty. Wall mass was 159 +/- 38 gm/m2 initially, decreased 25% to 116 +/- 29 gm/m2 at 4 month (p less than 0.001), and decreased a total of 34% to 105 +/- 33 gm/m2 at 8 months after valve repair. By 8 months not only was the mean wall mass within the normal range, but only three patients retained abnormal hypertrophy. Ejection fraction increased 8% (p = 0.06). Clinical function improved in all patients, with only three patients remaining outside of New York Heart Association functional class 1 at 8 months. Regression of ventricular mass into the normal range correlated with attainment of class 1 functional status (p less than 0.02), despite a lack of increase of ejection fraction. The single patient followed for 8 months after valvuloplasty had minor wall mass regression and minor clinical improvement.

Previous studies of the value of electrophysiologic studies in patients with nonsustained ventricular tachycardia (VT) have been hampered by the inclusion of a small number of patients with various types of heart disease. This retrospective study was designed to assess the value of programmed stimulation in 205 asymptomatic patients who had had an acute myocardial infarction greater than 1 month before study. Inclusion was based on 24-hour Holter monitoring during which patients had to manifest greater than or equal to 3 consecutive ventricular beats at a rate greater than 135 beats/min. Forty-seven (23%) patients had normal, 70 (34%) mildly impaired and 88 (43%) severely impaired left ventricular function. Programmed stimulation, using up to 3 extrastimuli, was used in each. Seventy-five patients (36%) were noninducible, 59 (29%) had nonsustained VT (less than 30 seconds), 67 (33%) had sustained monomorphic VT and 4 (2%) had either polymorphic VT or ventricular fibrillation. Eighty-two patients were not treated with antiarrhythmic drugs, 57 others were placed on a program selected empirically and 66 had therapy guided by electrophysiologic testing. Satisfactory follow-up information was gathered in 187 of the 205 patients, with a mean follow-up of 18 months. One hundred forty-two patients are alive and well, 39 had sustained VT or sudden death and 6 others had a cardiac death. Only left ventricular function discriminated those who had a sustained arrhythmia or died from those who did not. Thus, programmed stimulation did not have independent predictive value in patients with nonsustained VT. However, definitive conclusions can be reached only with a large prospective study carried out in untreated patients.

Electrophysiologic studies were performed in 83 consecutive patients with spontaneous nonsustained ventricular tachycardia (VT). VT was inducible in 52 patients (nonsustained VT only in 37 patients, nonsustained and sustained VT in 13 and sustained VT only in 2). During a follow-up of 3 to 111 months (mean 33), 10 patients died suddenly, 5 with coronary artery disease (CAD) and 5 with dilated cardiomyopathy. All patients with sudden death had an ejection fraction less than or equal to 0.40. Sudden death occurred in 4 of 15 patients with inducible sustained VT, 2 of 37 patients with only nonsustained VT and 4 of 31 patients without inducible VT. One patient with dilated cardiomyopathy and VT inducible only by isoproterenol died suddenly. Three of 5 patients with CAD who had sudden death had had inducible sustained VT, but 3 of 5 patients with cardiomyopathy who had sudden death had no inducible VT. Multivariate analysis revealed that patients with inducible sustained VT or an ejection fraction less than or equal to 0.40 had a 3-fold increased risk of sudden death, and patients with both factors had a 7-fold increased risk of sudden death. This study demonstrates that patients with nonsustained VT with an ejection fraction greater than 0.40 have an uncomplicated course; however, noninducibility does not predict such a course, particularly in patients with cardiomyopathy. The most powerful predictor of risk for sudden cardiac death is a left ventricular ejection fraction less than or equal to 0.40, but the presence of inducible sustained VT is an independent risk factor for sudden death.

The co-existence of horizontal and longitudinal dissociation of the atrioventricular (A-V) node has not previously been reported. Analysis of ECG tracings from 4 patients with supraventricular tachycardias showing an irregular ventricular rate suggest that such a mechanism was responsible for the irregular A-V conduction pattern. His bundle recording was obtained in one patient and revealed the site of block to be located in the A-V node. Multi-level block and longitudinal dissociation of the A-V node is probably not rare and should be included in the discussion of supraventricular arrhythmias displaying irregular ventricular rates.

Electrophysiological characteristics of the modes of initiation of 16 episodes of spontaneously occurring sustained ventricular tachycardia recorded in 16 patients by two-channel ambulatory electrocardiographic monitoring were compared with the characteristics of ventricular tachycardia induced by programmed electrical stimulation. Eleven episodes of spontaneous ventricular tachycardia began after a single ventricular premature depolarization (VPD), three episodes after two VPDs, and two episodes after five VPDs. By comparison, only four episodes of sustained ventricular tachycardia were induced with a single VPD. Each episode of spontaneous ventricular tachycardia was initiated by a late coupled VPD (RR':QT ratio greater than 1.0). The VPD was often morphologically similar to the ensuing ventricular tachycardia (eight of 11 episodes that began after a single VPD). No correlation was found between the modes of initiation of spontaneous and induced ventricular tachycardia. We hypothesize that concealed decremental slow conduction, reflected in the long coupling intervals of VPDs initiating ventricular tachycardia, is of critical importance in initiating ventricular tachycardia. We conclude that major differences exist in the timing and number of VPDs associated with the onsets of spontaneous and induced sustained ventricular tachycardia.

Left ventricular activation was studied in 21 patients: 7 with normal electrocardiograms (group I), 7 with prior transmural myocardial infarction (group II) and 7 with prior transmural myocardial infarction (MI) and recurrent sustained ventricular tachycardia (VT) (group III). Fragmented electrograms were defined as those less than 3 mV in amplitude and longer than 60 ms in duration. Such electrograms were found in no group I patients, 6 of 7 group II patients and all 7 group III patients. An average of 2 of the 12 sites mapped in each patient displayed fragmented electrograms in group II; an average of 6 of the 12 sites displayed fragmented electrograms in group III (p less than 0.01). Twelve of the 84 total sites mapped in group II displayed fragmented electrograms, whereas 39 of the 84 sites mapped in group III patients did (p less than 0.01). The longest fragmented electrogram found in the 6 group II patients in whom such electrograms were found was shorter in duration than the longest electrogram found in each of the 7 group III patients with fragmented electrograms (76 ms vs 135 ms, p less than 0.005). The duration of endocardial activation was longer in group II patients (79 +/- 7 ms) than in group I patients (39 +/- 4 ms, p less than 0.001). Duration of activation was also longer in group III patients (151 +/- 12 ms) than in either of the other groups (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Forty patients with sustained tachycardia occurring 3 to 65 days after myocardial infarction underwent programmed ventricular stimulation within 3 months of the infarction. Patients were characterized clinically by a complicated initial 48 hours of hospitalization for their acute infarction (85% of study group). The development of bundle branch block in association with infarction occurred with an unusually high frequency (32%). Ventricular tachycardia similar in configuration to spontaneous arrhythmia was induced with programmed ventricular stimulation in 33 (83%) of the 40 patients. In 15 (45%) of these 33 patients, additional morphologically distinct ventricular tachycardia not seen clinically was initiated. The induction of ventricular tachycardia was not significantly related to the time after myocardial infarction at which spontaneous ventricular tachycardia was initially observed. Only 20 of the 40 patients are alive after a mean follow-up period of 20 +/- 15 months. Twelve of the 20 deaths were sudden cardiac deaths. Sixteen of the 33 patients with inducible ventricular tachycardia died; 8 of the 16 deaths were sudden. By comparison, four of the seven patients with no inducible ventricular tachycardia died (probability [p] = not significant), all suddenly. The mode of therapy did not influence subsequent survival. It appears that in patients with sustained ventricular tachycardia occurring more than 48 hours after a recent myocardial infarction, ventricular tachycardia similar to that clinically observed can usually be induced by programmed stimulation. In addition, multiple morphologically distinct ventricular tachycardias, some of which have not been previously observed, are frequently induced. Finally, the prognosis for survival is poor, regardless of inducibility or mode of therapy, and may in part be related to a changing arrhythmia substrate.

The effects of cycle length and stimulation site on intraatrial conduction and refractoriness were evaluated in patients with and without atrial flutter (AFI) or fibrillation (AF) using the extrastimulus technique. Nineteen patients with spontaneous sustained AFI or AF were compared with 19 control patients. Programmed stimulation was performed at the right atrium and coronary sinus at drive cycle lengths of 600 and 450 ms. The atrial effective refractory period was similar in the patients with atrial dysrhythmias and the control group. The right atrial effective refractory period at a drive cycle length of 600 ms was significantly shorter in patients with AF (211 ms) than in patients with AFI (235 ms, p = 0.05). The conduction time of late (coupling intervals more than 50% of the drive cycle length) premature impulses was similar in the patients with atrial dysrhythmias and the control group. However, early extrastimuli (coupling intervals less than 50% of the drive cycle length) at a drive cycle length of 600 ms produced significantly more intraatrial conduction delay in the patients with atrial dysrhythmias than in the control patients. At a drive cycle length of 450 ms, similar delays in intraatrial conduction occurred in the patients with and without atrial dysrhythmias because of an increase in the maximal-observed intraatrial conduction delay in the control patients. This study shows that delay in conduction of early premature atrial stimuli at a drive cycle length of 600 ms is a marker of patients with spontaneous AFI and AF.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic studies were performed in 172 consecutive patients for evaluation of documented sustained ventricular tachyarrhythmias. One hundred thirteen patients presented with sustained ventricular tachycardia that was hemodynamically stable, and 59 patients presented with cardiac arrest. Seventy-one patients without previously documented or suspected ventricular arrhythmias were also studied to determine the specificity of our electrophysiologic study protocol. The stimulation protocol included single, double, and triple right ventricular extrastimuli and rapid ventricular pacing at multiple cycle lengths performed at one or more right ventricular sites. Stimulation was performed at one or more left ventricular sites in patients with documented spontaneous arrhythmias when right ventricular programmed stimulation failed to induce sustained ventricular tachycardia. Ventricular tachyarrhythmias were induced in 110 (97%) of the patients who presented with sustained ventricular tachycardia, in 48 (81%) of the patients who presented with cardiac arrest, and in 28 (40%) of the patients without documented spontaneous arrhythmias. Right ventricular triple extrastimuli induced tachycardia in 22% of patients who presented with sustained ventricular tachycardia vs 46% of those who presented with cardiac arrest (p less than .001). Left ventricular stimulation was required for tachycardia induction in 3% of patients with stable tachycardia vs 19% of those with cardiac arrest (p less than .01). Triple extrastimuli induced 57% of tachycardias in the 28 patients without spontaneous arrhythmias, and virtually all of these tachycardias were polymorphic and nonsustained. The cycle lengths of tachycardias induced in each group by double and triple extrastimuli were similar, but the tachycardias induced in patients with cardiac arrest were significantly faster than those induced in the ventricular tachycardia group (mean cycle length 218 vs 291 msec, p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Programmed ventricular stimulation (PVS) was prospectively performed in 56 consecutive patients from both the right ventricular (RV) apex and the RV outflow tract. Thirty-seven patients had documented clinical sustained ventricular tachycardia (VT) and 19 patients had no sustained spontaneous VT in the absence of antiarrhythmic drugs. The sensitivity of VT induction was 65% from the RV apex, 76% from the RV outflow tract and was 89% with combined stimulation at both RV sites. The specificity from the RV apex, the RV outflow tract and both sites combined was 100%. When sustained VT was induced from both sites (51%), it was usually of the same morphologic characteristics, axis and cycle length. When sustained VT was induced at 1 site and nonsustained VT at the second site, the morphologic characteristics or axis usually differed. Of patients who had VT induced at both RV sites during the baseline study 37% had VT rendered noninducible during treatment with conventional antiarrhythmic agents. No patients whose VT was induced at only 1 RV site responded to conventional drugs. We conclude that programmed ventricular stimulation at a second RV site is frequently helpful in the evaluation of VT. Inducibility at only 1 of 2 RV sites predicts a poor response to conventional antiarrhythmic drugs.

The effectiveness of verapamil in controlling ventricular rate was evaluated in 20 patients with atrial fibrillation or flutter with a rapid ventricular response (Group 1) and 30 patients with paroxysmal supraventricular tachycardia (Group 2). In Group 1 low-dose verapamil (0.075 mg/kg body weight) decreased the mean ventricular rate from 146 to 114 beats/min (p < 0.01) compared to a decrease of 145 to 132 beats/min (p < 0.01) after placebo. In Group 2, 14 of 29 patients converted to sinus rhythm after low-dose verapamil, nine of 15 after high-dose verapamil (0.15 mg/kg body weight), and one of 24 after placebo (p < 0.01). We conclude that verapamil results in a clinically significant slowing of the ventricular response in atrial fibrillation or atrial flutter and is superior to placebo for conversion of paroxysmal supraventricular tachycardia to sinus rhythm.

We have evaluated the influence of several factors on the binding of disopyramide to protein in human serum using a new ultrafiltration system and the enzyme multiplied immunoassay technique (EMIT) for disopyramide immunoassay. From these studies and those of other investigators, we conclude that the most significant in vivo factors influencing disopyramide binding in human serum are total disopyramide concentration, the concentration of alpha 1-acid glycoprotein, and the concentration of mono-N-dealkyldisopyramide. Significant variation in binding occurs in patients whose total disopyramide concentration is within the therapeutic range. The proportion of free disopyramide ranged from 16% to 54% in the sera of 50 cardiac patients whose total disopyramide concentration ranged from 0.5 to 5.8 mcg/ml. Since there is so much variation in the proportion of disopyramide that is free, and since it is the unbound form of the drug that is pharmacologically active, it is likely in patients whose arrhythmia responds to disopyramide therapy that unbound drug concentration will be a better indicator of drug efficacy and toxicity than will be total drug concentration. To test this hypothesis, we are investigating the relationship between steady state total and unbound disopyramide plasma levels in patients with supraventricular or ventricular arrhythmias, and pharmacologic response as determined by standard intracardiac electrophysiologic studies.

To determine the potential for myocardial injury during electrophysiologic study for ventricular arrhythmia, total creatine kinase and creatine kinase B-subunit enzyme activity were serially measured after the procedure in 24 patients. During electrophysiologic study 14 of the 24 patients had sustained ventricular tachycardia or fibrillation, 4 patients had nonsustained ventricular tachycardia, and 6 patients had no ventricular arrhythmia induced. Cardioversion was necessary because of hemodynamic collapse in 9 of the 14 patients with sustained ventricular tachycardia or ventricular fibrillation. Coronary heart disease was present in 14 of the 24 patients, in 9 of the 14 with sustained ventricular tachycardia or ventricular fibrillation, and in 7 of the 9 patients requiring cardioversion. Total creatine kinase was modestly elevated (greater than twice baseline or greater than normal, or both) 24 hours after electrophysiologic study in 10 (42%) of the patients. Electrophysiologic study with or without the induction of ventricular tachycardia or ventricular fibrillation was not associated with increased creatine kinase B-subunit activity even in patients with coronary heart disease.

The efficacy of disopyramide in the management of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) was evaluated in 50 patients by programmed ventricular stimulation: 38 patients had coronary artery disease (16 with left ventricular aneurysm), 8 had other cardiac diseases, and 4 had no apparent heart disease. Disopyramide was administered orally for 72 hours (dosage 400 to 1,600 mg/day), resulting in a plasma level of 3.6 +/- 1.2 micrograms/ml (mean +/- standard deviation [SD]). Disopyramide prevented induction of sustained ventricular tachyarrhythmias in 17 patients (34%) and failed to prevent induction in 33 patients (66%). Plasma levels were not significantly different regardless of response to disopyramide. The VT cycle length in patients responding to disopyramide was shorter than in nonresponding patients (225 +/- 51 ms versus 281 +/- 70 ms, p = 0.005). Disopyramide increased VT cycle length in those patients in whom it was ineffective (failed to prevent induction) from 281 +/- 70 ms to 347 +/- 64 ms (p less than 0.001). Ventricular refractory periods, QRS, and QTc durations significantly increased after disopyramide administration. Of the 17 patients in whom tachyarrhythmias were noninducible on disopyramide, 11 were discharged on disopyramide and followed up for 19 +/- 9 months; 9 of them remained free of VT. Heart failure developed in 2 of these patients. One other patient in whom disopyramide was ineffective had irreversible heart failure and died. It is concluded that disopyramide (1) prevents induction of ventricular tachyarrhythmias in one third of patients studied and remains clinically effective in approximately 80%, (2) is more frequently effective in rapid tachycardias, (3) prolongs the VT cycle length when ineffective, and (4) may produce marked hemodynamic embarrassment in patients with significant left ventricular dysfunction.

The efficacy of a recently developed programmable implantable pacemaker which can be used in the management of supraventricular tachycardias (with, or without, associated bradyarrhythmias) was evaluated in the cardiovascular laboratory and at the bedside in the coronary care unit. Although this pacemaker functions primarily in a DVI-DVO mode, it was also made (iatrogenically) to operate in a DOO mode. The study was performed in six patients with reciprocating atrioventricular tachycardias (four of the long P-R--short R-P type and two of the short P-R--long R-P type). Both DVI-DVO and DOO pacing abolished all episodes of tachycardia in five of the patients. However, DOO pacing was also capable of initiating episodes of tachycardia in two of the six patients. The events observed in two of the patients raise the possibility that (reversed) ventriculoatrial sequential pacing may be required in some tachycardias of the short P-R--long R-P type. This preliminary study suggests that programmability of pacing modes, rates, and intervals is a desirable feature that pacemakers used to manage drug-resistant tachycardias should have.

Eleven consecutive patients with idiopathic dilated cardiomyopathy and spontaneous, sustained ventricular tachycardia (VT) of uniform morphology underwent programmed ventricular stimulation and serial antiarrhythmic drug testing. The mean ejection fraction was 30 +/- 6.4%. Sustained VT was induced by programmed electrical stimulation in all 11 patients. A mean of 3.7 +/- 2.4 antiarrhythmic drugs were evaluated by programmed stimulation, including at least one experimental agent in eight patients. In nine of 11 patients VT remained inducible on all drug therapy. During a mean follow-up period of 21 +/- 14 months there were four sudden deaths and two patients with recurrences of VT. In all six patients with sudden death or recurrence of VT, the arrhythmia remained inducible on drug therapy. Three patients who died suddenly had a hemodynamically stable, induced tachycardia on antiarrhythmic therapy. Of eight patients treated with amiodarone, only two were successfully treated. We conclude that in patients with sustained VT and idiopathic dilated cardiomyopathy, VT can be induced by programmed electrical stimulation. VT will usually remain inducible on antiarrhythmic therapy, and sudden death can occur despite slowing and improved tolerance of the induced arrhythmia. Amiodarone may have limited efficacy, and more aggressive therapy, such as surgery or implantation of an automatic internal defibrillator, should be considered in this patient population.

Electrophysiologic studies were performed in 119 survivors of cardiac arrest. Sustained ventricular arrhythmias were initiated by programmed ventricular stimulation in 72 patients (61%). Coronary artery disease patients with induced sustained ventricular arrhythmias had a higher incidence of prior myocardial infarction (95 versus 72%) and ventricular aneurysm (59 versus 28%) and a lower ejection fraction (37 versus 50%) than those with no inducible sustained ventricular arrhythmias. Of the 72 patients with inducible ventricular arrhythmias, 11 (15%) died suddenly during a mean follow-up of 18 months (range 15 days to 58 months). In this group, 6 of 41 patients (15%) discharged on a successful antiarrhythmic regimen and 5 of 27 patients (19%) discharged on an unsuccessful regimen or without a predischarge study have died suddenly. Of these 27 patients, 1 of 12 patients treated with amiodarone and 4 of 15 (27%) with conventional antiarrhythmic therapy died suddenly. The remaining 4 patients died of nonarrhythmic causes in the postoperative period. Of 47 patients without inducible sustained ventricular arrhythmias, 15 (32%) died suddenly at a mean follow-up of 20 months, 10 (34%) with and 15 (28%) without empiric therapy. It is concluded that sustained ventricular arrhythmias can be initiated in most patients resuscitated from cardiac arrest. Patients with inducible arrhythmias have greater left ventricular dysfunction than those without inducible arrhythmias. Medical or surgical therapy that prevented the induction of sustained ventricular arrhythmias was predictive of a successful outcome in 85% of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)

This report describes a case of pacemaker-mediated tachycardia from a single chamber temperature sensitive rate modulated pacemaker. The patient experienced diaphragmatic pacing that produced an increase in right ventricular blood temperature. This temperature increase was sensed by the pacemaker and led to sustained upper rate limit pacing. Decreasing the ventricular output to prevent diaphragmatic capture eliminated further episodes of pacemaker-mediated tachycardia.

The effect of increased stimulus current strength on the right ventricular effective refractory period during sustained ventricular tachycardia and on the ability of single premature right ventricular stimuli to terminate ventricular tachycardia was evaluated. Studies were performed during 53 episodes of sustained ventricular tachycardia in 25 patients. Forty-four of 53 episodes were slowed by pharmacologic therapy. Current intensities of twice diastolic threshold, 5 mA and 10 mA were used. Increasing current from twice diastolic threshold (1.52 +/- 0.66 mA) to 5 mA (32 episodes) shortened the mean ventricular effective refractory period from 213 +/- 50 to 188 +/- 43 msec (p less than 0.001); and from twice diastolic threshold (1.53 +/- 0.60 mA) to 10 mA (42 episodes), from 206 +/- 55 to 176 +/- 50 msec (p less than 0.001). There was a direct correlation between cycle length of ventricular tachycardia and the ventricular effective refractory period measured at twice diastolic threshold (r = 0.77, p less than 0.001). However, the cycle length of ventricular tachycardia and the amount of shortening of ventricular effective refractory period as current was increased were not significantly correlated (r = 0.40). Eleven episodes of ventricular tachycardia (21%) that could not be terminated by ventricular stimulation at twice diastolic threshold were terminated when increased current strength was used. The ability to terminate ventricular tachycardia was associated with a decrease in ventricular effective refractory period and long tachycardia cycle length. The mean cycle length of the 11 episodes terminated was 455 +/- 50 msec, compared with 381 +/- 63 msec in the 42 episodes not terminated at increased current.

Ventricular extrastimuli or rapid ventricular pacing used to terminate ventricular tachycardia (VT) may be ineffective or may accelerate VT. Therefore, a new method to facilitate termination of VT and decrease the incidence of acceleration was evaluated. The new method utilized rapid ventricular pacing at cycle length 10 to 100 ms shorter than VT cycle length with the introduction of 1 or 2 ventricular extrastimuli. The efficacy of this combination method in terminating VT was assessed in 25 patients in whom ventricular extrastimuli and rapid ventricular pacing at cycle lengths and coupling intervals comparable with those used in the new method were unsuccessful. This combination method successfully terminated VT in 21 of 25 patients with cycle lengths of 230 to 400 ms. VT was terminated in 6 of 8 patients receiving drugs in whom VT could not be terminated by 1 to 2 ventricular extrastimuli or rapid ventricular pacing; in 6 of 8 patients unresponsive to ventricular extrastimuli and in whom rapid ventricular pacing produced acceleration of VT; and in 9 of 9 patients in whom antiarrhythmic agents made VT unresponsive to ventricular extrastimuli or rapid ventricular pacing. A combination of rapid pacing and extrastimuli can terminate VT unresponsive to ventricular extrastimuli or rapid ventricular pacing alone and may avoid acceleration of VT using rapid ventricular pacing at very short cycle lengths for termination.

Thirty-three patients with sustained ventricular arrhythmias underwent electrophysiologic testing after intravenous and again after oral procainamide administration. Two groups were identified: group 1 included 15 patients with concordant serum procainamide concentrations with less than a 3 micrograms/ml difference after intravenous (mean 8.6 +/- 2.7) and oral (mean 8.8 +/- 2.7) procainamide administration, with mean N-acetylprocainamide concentrations of 1.0 +/- 0.6 and 6.2 +/- 2.8 micrograms/ml, respectively. Group 2 included 18 patients with discordant serum procainamide concentrations after intravenous (mean 9.5 +/- 5.9 micrograms/ml) and oral (mean 14.1 +/- 5.2 micrograms/ml) procainamide, with mean N-acetylprocainamide concentrations of 0.9 +/- 0.5 and 10.7 +/- 5.7 micrograms/ml, respectively. In group 1, response to programmed stimulation was the same after intravenous and oral procainamide administration, with no inducible ventricular arrhythmia in 5 of 15 patients. In group 2, 3 of 18 patients had no inducible arrhythmia after intravenous compared with 7 of 18 patients after oral procainamide administration. There was a different response to programmed stimulation after oral compared with intravenous procainamide in 6 of 18 patients in group 2 but in none of 15 patients in group 1 (p = 0.02). The effective procainamide concentration was greater than the ineffective concentration in five of the six patients with a discordant response, and the effective route of administration was oral in five of the six patients. The change in ventricular refractoriness in group 1 was similar after intravenous (28 +/- 23 ms) and oral (29 +/- 19 ms) procainamide, whereas in group 2, refractoriness was increased more after oral (33 +/- 21 ms) than intravenous (20 +/- 17 ms) procainamide administration and paralleled the difference in procainamide concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

The mode of termination of ventricular tachycardia (VT) and its relation to tachycardia cycle length was evaluated in 139 patients. Tachycardia was terminated by programmed stimulation in 110 patients (79%) and cardioversion was required in 29 patients (21%). Single, double, and triple ventricular extrastimuli terminated the tachycardia in 23 of 85 (27%), 39 of 62 (63%), and 7 of 16 patients (44%), respectively. In all patients requiring 1 extrastimulus, in 35 patients (90%) requiring 2 extrastimuli, and in 6 patients (86%) requiring 3 extrastimuli, the tachycardia cycle length exceeded 300 ms. Rapid ventricular pacing terminated tachycardia in 41 of 54 patients (76%). In 21 (51%) of these patients the tachycardia cycle length exceeded 300 ms. However, rapid ventricular pacing caused acceleration of the arrhythmia in 19 patients (35%). The ability of procainamide to modify the termination of VT was studied in 23 patients. In 7 of these patients (30%) procainamide increased the tachycardia cycle length by 49 +/- 42 ms (p less than 0.01) and did not modify the mode of termination. In 6 patients (26%) procainamide increased cycle length by 142 +/- 108 ms (p less than 0.01), but termination was more difficult. In 10 patients (44%) procainamide increased the cycle length by 138 +/- 110 ms (p less than 0.001) and termination was easier. We conclude that termination of VT by timed extrastimuli requires a tachycardia cycle length longer than 300 ms. Rapid pacing or cardioversion is usually required when the cycle length is less than 300 ms. Although procainamide slows tachycardia, it can unpredictably make termination more difficult in 1 of 4 patients.

We evaluated 126 patients with inducible sustained ventricular tachyarrhythmias to assess whether the response to procainamide during electrophysiologic study could predict responses to other conventional antiarrhythmic agents and combinations of agents. Thirty of 42 patients in whom tachycardia was not inducible after the administration of procainamide and 69 of 84 patients in whom ventricular tachycardia was inducible after procainamide underwent serial electrophysiologic studies. Forty-three of 67 antiarrhythmic regimens (64%) tested in the patients in whom ventricular tachycardia could not be induced after procainamide prevented induction of ventricular tachycardia, compared with 10 of 145 regimens (7%) tested in the patients in whom ventricular tachycardia could be induced after procainamide. Sixty of the 69 patients in whom ventricular tachycardia remained inducible after procainamide had ventricular tachycardia induced on all other conventional antiarrhythmic regimens tested. By comparison, of the 30 patients in whom ventricular tachycardia became noninducible after procainamide, 25 had no ventricular tachycardia inducible on at least one other antiarrhythmic regimen tested. Thus, the response to procainamide accurately predicted the response to other conventional antiarrhythmic agents during electrophysiologic study.

Traditionally, surgical therapy for tachydysrhythmias has been reserved for drug-refractory cases. Accordingly, there has been no study comparing medical with surgical therapy in similar groups of patients. Recent developments in surgical therapy for supraventricular and ventricular tachydysrhythmias have resulted in lower morbidity and mortality with good surgical success. In most patients with the Wolff-Parkinson-White syndrome, accessory pathway division can be performed with very low mortality and high chance for success, obviating the need for lifelong drug therapy. Similarly, in patients with life-threatening ventricular tachydysrhythmias, several operative techniques including the encircling endocardial ventriculotomy and subendocardial resection offer an alternative to therapy which often requires frequent dosing with one or more medications, each associated with a significant incidence of adverse effects. These newer operative techniques for both supraventricular and ventricular tachydysrhythmias are challenging the widely held concept that surgery should be reserved only for patients with drug-refractory tachydysrhythmias.

The antiarrhythmic efficacy of mexiletine was evaluated in 44 patients with drug-resistant ventricular tachyarrhythmias. In 33 of these patients, the efficacy of mexiletine was assessed on the basis of the results of programmed ventricular stimulation. Mexiletine did not alter the ventricular effective refractory period, the Q-Tc interval, or the methods of tachyarrhythmia induction and termination during programmed stimulation. The mean cycle length of ventricular tachycardia (VT) increased from 270 +/- 49 to 313 +/- 80 ms in 21 patients in whom VT remained inducible on mexiletine alone (p less than 0.002). Overall, VT remained inducible with methods similar to control (no drugs) inductions in 25 patients receiving mexiletine alone or in combination with a type I agent. VT induction was prevented in only 8 patients, 3 on mexiletine alone and 5 receiving mexiletine combined with another drug. Mexiletine alone (in 2 patients) or with another agent (in 3) suppressed clinical recurrence of VT in an additional 5 of 11 patients who did not undergo electrophysiologic study. These 13 patients were discharged on mexiletine alone (5 patients) or in combination with other drugs (8 patients), and remained arrhythmia-free over a mean follow-up period of 7.7 +/- 4.1 months. Adverse effects occurred in 27 of 44 patients (61%) and were gastrointestinal in 17 and/or neurologic in 22. The drug was discontinued because of adverse effects in 6 patients (14%). Thus, mexiletine has limited efficacy when used alone, but when combined with other drugs it may be useful in up to 30% of patients with drug-resistant ventricular arrhythmias. Adverse effects are relatively common.