Prediction of sustained ventricular tachycardia inducible by programmed stimulation in patients with coronary artery disease. Utility of clinical variables.

BACKGROUND: Cardiologists often use clinical variables to determine the need for electrophysiological studies to stratify patients for risk of sudden death. It is not clear whether this is rational in patients with coronary artery disease, left ventricular dysfunction, and nonsustained ventricular tachycardia. METHODS AND RESULTS: We analyzed the first 1721 patients enrolled in the Multicenter UnSustained Tachycardia Trial to determine whether clinical variables could predict which patients would have inducible sustained monomorphic ventricular tachycardia. The rate of inducibility of sustained ventricular tachycardia was significantly higher in patients with a history of myocardial infarction and in men compared with women. There was a progressively increased rate of inducibility with increasing numbers of diseased coronary arteries. There was a significantly lower rate of inducibility in patients with prior coronary artery bypass surgery and in patients who also had noncoronary cardiac disease. The rate of inducibility was higher in patients of white race, patients with recent (

Recanalization of chronically occluded aortocoronary saphenous vein bypass grafts by extended infusion of urokinase: initial results and short-term clinical follow-up.

Chronic occlusion of saphenous vein aortocoronary bypass grafts is a common problem. Although percutaneous transluminal angioplasty of a saphenous vein with a stenotic lesion is feasible, angioplasty alone of a totally occluded vein graft yields uniformly poor results. Patients with such occlusion are often subjected to repeat aortocoronary bypass surgery. Experience with a new technique that allows angioplasty to be performed in a totally occluded saphenous vein bypass graft is reported. This technique utilizes infusion of prolonged low dose urokinase directly into the proximal portion of the occluded graft. Forty-six consecutive patients with 47 totally occluded grafts were studied. Patients had undergone end to side saphenous vein bypass grafting 1 to 13 (mean 7) years previously. All patients presented with new or worsening angina pectoris with ST-T changes or non-Q wave acute myocardial infarction and all had a totally occluded saphenous vein bypass graft. The new technique entailed the positioning of an angiographic catheter into the stub of the occluded graft and the advancement of an infusion wire into the graft. Patients were returned to the coronary care unit, where urokinase was delivered at a dose of 100,000 to 250,000 U/h. The total dose of urokinase ranged from 0.7 to 9.8 million U over 7.5 to 77 h (mean 31). After therapy, recanalization was seen in 37 (79%) of the 47 grafts. In 20 successfully treated patients, angiography was performed 1 to 24 (mean 11) months after treatment; 13 (65%) of these grafts were patent.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of the resetting phenomenon in sustained uniform ventricular tachycardia: incidence and relation to termination.

UNLABELLED: Although the phenomenon of resetting has been studied in several experimental and clinical rhythms, it has not been systematically analyzed in ventricular tachycardia. To define the incidence and determinants of resetting as well as its relation to ventricular tachycardia termination, the response to programmed stimulation was prospectively studied during 78 electrically induced episodes of sustained, uniform ventricular tachycardia (mean cycle length 365 +/- 59 ms) in 53 patients. Single and double ventricular extrastimuli were introduced during 78 and 39 episodes of ventricular tachycardia, respectively. Rapid ventricular pacing was performed during 27 episodes. Resetting occurred in response to single ventricular extrastimuli in 43 (55%) of 78 ventricular tachycardias, to double extrastimuli in 31 (79%) of 39 ventricular tachycardias and to rapid pacing in 23 (85%) of 27 ventricular tachycardias. No ventricular tachycardia characteristic distinguished those tachycardias that were reset from those not reset. Termination of ventricular tachycardia occurred in 7 (9%) of 78 episodes with single ventricular extrastimuli, 14 (36%) of 39 episodes with double ventricular extrastimuli and 13 (48%) of 27 episodes with rapid pacing. Termination was less frequent than resetting with both single (9 versus 55%) and double (36 versus 79%) extrastimuli, as well as rapid pacing (48 versus 85%). Resetting preceded termination in 7 of 7 ventricular tachycardias terminated with single ventricular extrastimuli, 12 of 14 terminated with double ventricular extrastimuli and 9 of 13 terminated by rapid pacing. Ventricular tachycardias that were terminated could not be differentiated from those that were reset without termination. IN CONCLUSION: Resetting with programmed extrastimuli is common in hemodynamically stable sustained ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Coupling intervals of ventricular extrastimuli causing resetting of sustained ventricular tachycardia secondary to coronary artery disease: relation to subsequent termination.

Single and double ventricular extrastimuli (VE) delivered during sustained, uniform ventricular tachycardia (VT) are able to reset or terminate the tachycardia. The relation between the coupling intervals of single and double VE resetting VT and those terminating it was examined in 80 uniform, morphologically distinct VT occurring in 52 patients. Of the 80 tachycardias receiving single VE, 41 were reset and 8 terminated. The corrected coupling interval of single VE first causing resetting was 0.81 +/- 0.08 compared with 0.66 +/- 0.06 for termination (p less than 0.001). Forty-two tachycardias received double VE with 33 being reset and 13 terminating. The corrected coupling interval of double VE at which resetting was first seen was 0.86 +/- 0.08 compared with 0.73 +/- 0.05 for termination (p less than 0.001). If the longest corrected coupling interval causing resetting was greater than or equal to 0.75, then 7 of 34 tachycardias terminated with single VE and 13 of 31 terminated with double VE compared with only 1 of 46 terminating with single VE and 0 of 10 with double VE if resetting was not observed by a corrected coupling interval of 0.75 (p less than 0.01 and p less than 0.02, respectively). If the longest corrected coupling interval at which resetting occurred was greater than or equal to 0.75, the predictive value for VT termination was 21% with single VE and 42% with double VE compared with only 2% with single VE and none with double VE if resetting was not observed by this corrected coupling interval.(ABSTRACT TRUNCATED AT 250 WORDS)

The resetting response of ventricular tachycardia to single and double extrastimuli: implications for an excitable gap.

UNLABELLED: To evaluate the influence of local tissue refractoriness and delay in intervening tissue on the ability of single ventricular extrastimuli to reset and characterize a resetting response pattern in ventricular tachycardia (VT), single ventricular extrastimuli were delivered during 81 VTs and double ventricular extrastimuli in 45 of the 81 VTs. Resetting of VT was recognized as a less than fully compensatory pause after stimulation and was seen in 43 of 81 VTs (53%) with single ventricular extrastimuli and 35 of 45 (78%) with double ventricular extrastimuli. Double ventricular extrastimuli reset 16 VTs not reset by single ventricular extrastimuli. The return cycle, the interval from the extrastimulus to the first VT beat after extrastimuli, has 1 of 3 distinct response patterns: flat, increasing, and flat plus increasing. In 19 VTs, resetting was seen with both single ventricular extrastimuli and double ventricular extrastimuli; 4 flat responses with single ventricular extrastimuli became flat plus increasing with double ventricular extrastimuli. All other patterns were unchanged. In the 19 VTs reset by both single and double ventricular extrastimuli, the estimate of both the total reset zone (94 +/- 36 vs 56 +/- 32 ms) and the flat portion of the reset zone (52 +/- 42 vs 42 +/- 28 ms) was significantly longer with double ventricular extrastimuli (p less than 0.001 and p less than 0.02, respectively). IN CONCLUSION: (1) when single ventricular extrastimuli failed to reset a VT, double ventricular extrastimuli from the same site may reset the VT.

Influence of the site of stimulation on the resetting phenomenon in ventricular tachycardia.

Uniform, sustained ventricular tachycardia (VT) in the setting of prior myocardial infarction is believed to be due to reentry. The ability to reset VT with programmed extrastimuli requires that the premature impulse reach and enter the reentrant circuit. To evaluate the importance of the site of pacing on the ability to reset VT, single ventricular extrastimuli were delivered during 32 morphologically distinct, uniform VTs from both the right ventricular (RV) apex and RV outflow tract. Single ventricular extrastimuli resulted in resetting of VT from the RV apex only in 6 VTs, from the RV outflow tract only in 2, from both sites in 11 VTs and neither site in 13. When VT reset at both RV sites, 1 RV site or neither RV site was compared, a left bundle branch block VT QRS morphologic pattern was found to be more common in VT reset at both sites than at neither site (8 of 11 vs 4 of 13, p less than 0.05). No other differences in VT characteristics analyzed were found between these groups. Multiple ventricular extrastimuli were delivered in 16 VTs; in 6 of these, resetting was shown from at least 1 additional site, as compared to the response with single ventricular extrastimuli. In summary, site of stimulation can influence the ability of premature extrastimuli to reset uniform VT, and site dependence of VT resetting diminishes when multiple extrastimuli are used. This suggests that refractoriness or conduction delay in tissue between the pacing site and tachycardia circuit are important determinants of ability to reset VT from a particular site.

Procainamide-induced slowing of ventricular tachycardia with insights from analysis of resetting response patterns.

To investigate the mechanism of slowing of the rate of ventricular tachycardias (VTs) by procainamide, resetting response patterns were characterized in 24 VTs in 22 patients. All patients had coronary artery disease and inducible sustained VT during procainamide therapy. Only tachycardias with the same surface QRS morphology before and after procainamide were studied: all were slowed by procainamide. The mean cycle length was 292 +/- 61 ms before and 374 +/- 61 ms after procainamide (p less than 0.05). The mean effective refractory period, measured at the right ventricle, was 241 +/- 21 ms before and 261 +/- 24 ms after procainamide (p less than 0.05). During procainamide therapy, single and double extrastimuli were delivered during VT and resetting response patterns identified. Patterns were characterized as flat, increasing or flat plus increasing. Resetting was seen in 17 (71%) of these VTs and resetting response patterns were identified in 16 (94%) of these. The resetting response pattern was flat in 7, flat plus increasing in 5 and increasing in 4. The finding of some flat portion at the end of resetting response patterns in 12 VTs after procainamide indicates that the reentrant impulse conducts through fully recovered tissue within the circuit. It suggests that procainamide slowed these VTs by slowing conduction velocity in fully recovered tissue due to sodium channel blockade and not by prolongation of action potentials and refractory periods.

Cardiac amyloidosis causing ventricular tachycardia. Diagnosis made by endomyocardial biopsy.

In patients with malignant ventricular arrhythmias, endomyocardial biopsy may be helpful when all other findings from the workup are negative. A case of nonsustained polymorphic ventricular tachycardia is presented. The findings from an echocardiogram, coronary angiogram, and cardiac catheterization were negative. An electrophysiologic study showed inducible nonsustained ventricular tachycardia. A right ventricular endomyocardial biopsy was diagnostic of cardiac amyloid. The findings from a workup for systemic amyloidosis were negative. Primary cardiac amyloidosis should be considered in patients with malignant arrhythmias and no documented heart disease, and endomyocardial biopsy is helpful in making this diagnosis.

Atrial fibrillation: a risk factor for increased mortality--an AVID registry analysis.

Emerging evidence suggests that atrial fibrillation is not a benign arrhythmia. It is associated with increased risk of death. The magnitude of association is controversial and potential causes remain unknown. Patients in the registry of the Antiarrhythmics Versus Implantable Defibrillators (AVID) Trial form the basis for this report. Baseline variables, in particular the presence or absence of a history of atrial fibrillation/flutter, were examined in relation to survival. Multivariate Cox regression was used to adjust for differences in important baseline co-variables using 27 pre-selected variables. There were 3762 subjects who were followed for an average of 773+/-420 days; 1459 (39 %) qualified with ventricular fibrillation and 2303 (61 %) with ventricular tachycardia. A history of atrial fibrillation/flutter was present in 24.4 percent. There were many differences in baseline variables between those with and those without a history of atrial fibrillation/flutter. After adjustment for baseline differences, a history of atrial fibrillation/flutter remained a significant independent predictor of mortality, (relative risk=1.20; 95 % confidence intervals=1.03-1.40; p=0.020). Antiarrhythmic drug use, other than amiodarone or sotalol, was also a significant independent predictor of mortality (relative risk 1.34; 95 % confidence intervals 1.07-1.69, p=0.011. Atrial fibrillation/flutter is a significant independent risk factor for increased mortality in patients presenting with ventricular tachyarrhythmias. This risk may have been overestimated in previous studies that could not adjust for the proarrhythmic effects of antiarrhythmic drugs other than amiodarone or sotalol.

A system approach to intravenous thrombolysis in acute myocardial infarction in community hospitals: the influence of paramedics.

UNLABELLED: During a 3-year period, intravenous streptokinase (IV STK) was given to 110 consecutive patients ages 34-78 in the course of acute myocardial infarction (AMI) in three community hospitals served by the same paramedic system. 1.5 million units of IV STK was given over 30 minutes. Half of the patients were brought to the hospital by paramedics. The average time from onset of pain to administration of IV STK was 107 minutes in the paramedic group and 182 minutes for the others. Of 110 patients, 98 (89%) showed clinical evidence of reperfusion and 94 of 106 patients (89%) showed angiographic reperfusion. Angiography was performed from 1 to 10 days post-AMI. Mean time to angiography was 6 days for the first 58 patients and 2 days for the last 52 patients. In-hospital mortality was 2 of 110 patients and there was 1 late death at 8 months for an overall 3-year mortality 2.7%. Of 86 patients, 83 (96%) working before their infarct are working now. Of 107 survivors, 96 (90%) are Functional Class I. CONCLUSIONS: (1) IV STK is safely administered in a high percentage of AMI patients. (2) IV STK is safely administered in community hospitals. (3) Paramedics act as an early warning system and allow for earlier treatment than patients presenting without paramedic involvement. (4) Successful coronary reperfusion with IV STK results in low mortality rates and minimizes functional disability. (5) A system-wide approach to reducing time to treatment in AMI may be the most influential factor in affecting morbidity and mortality.

Diagnosis of coronary sinus diverticulum in Wolff-Parkinson-White syndrome using coronary angiography.

The entity of Wolff-Parkinson-White Syndrome and coronary sinus diverticula when the bypass tract is posteroseptal in location has been described recently. The presence of this diverticulum may complicate arrhythmia surgery and could potentially add to the risk of catheter ablation. We describe a case of Wolff-Parkinson-White Syndrome in which the diagnosis of a coronary sinus diverticulum was made preoperatively using late-phase coronary angiography and suggest angiography be considered in patients with posteroseptal bypass tracts prior to surgery or catheter ablation.

Transient complete heart block during radiofrequency ablation of a left lateral bypass tract.

RF catheter ablation of accessory bypass tracts associated with the Wolff-Parkinson-White syndrome has become an accepted and widespread therapy. When bypass tracts are located in the free wall of the left ventricle, a single catheter technique may be utilized. A single catheter is placed via the femoral artery, across the aortic valve into the left ventricle. Mapping is performed during sinus rhythm, and ablation performed at the site of recording of Kent bundle activation. We describe a case of a patient with Wolff-Parkinson-White syndrome presenting with rapid atrial fibrillation requiring cardioversion. This patient subsequently underwent catheter ablation of a left free-wall bypass tract using the single catheter technique. At baseline, preexcitation and right bundle branch block (RBBB) were present on the ECG. During catheter ablation of the accessory pathway, transient complete AV block was seen. This was felt likely to be due to trauma to the His bundle, or more likely to the left bundle branch, as the ablation catheter crossed the aortic valve. The bypass tract was successfully ablated after placement of a temporary right ventricular pacemaker. AV conduction resumed with a pattern of RBBB. A temporary right ventricular pacing catheter should be placed prior to RF ablation of left-sided bypass tracts when the ECG is also suggestive of RBBB.

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

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

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

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

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

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