Cardiovascular collapse caused by electrocardiographically silent 60-Hz intracardiac leakage current. Implications for electrical safety.

BACKGROUND: The national standard for safe 60-Hz intracardiac leakage current under a single-fault condition is 50 microA. This standard is intended to protect patients from alternating current (AC) at levels below the threshold for sensation, but the minimum unsafe level for AC in closed-chest humans is not known. To determine this value, we studied 40 patients at testing of implantable cardioverter-defibrillators using a programmable source of 60-Hz AC. METHODS AND RESULTS: We applied AC for 5-second test periods in increasing strengths until ventricular fibrillation (VF) was induced or 1 mA was reached. Two current paths were tested: bipolar, between tip and ring electrodes of a right ventricular pacing catheter, and unipolar, from tip to a remote electrode. We observed a characteristic sequence of 3 responses as AC was increased: (1) intermittent ventricular capture with QRS morphology identical to pacing through the electrodes (minimum value, 20 microA); (2) continuous capture at cycle length 282+/-88 ms (minimum value, 32 microA); and (3) VF persisting after AC termination (minimum value, 49 microA). Continuous capture caused loss of pulsatile arterial pressure and cardiovascular collapse (mean arterial pressure, 32+/-8 mm Hg) for the duration of AC with no ECG evidence of AC stimulation. Thus, the clinical picture was that of hypotensive ventricular tachycardia (VT). The continuous-capture threshold was /=5 seconds should be

Efficacy and safety of sotalol in patients with refractory atrial fibrillation or flutter.

Sotalol's usefulness in treatment of atrial fibrillation and atrial flutter is unproven. This study evaluated (1) the efficacy of sotalol in preventing recurrences of paroxysmal atrial fibrillation or atrial flutter and controlling ventricular rate (in chronic atrial fibrillation or relapse of paroxysmal atrial arrhythmias), (2) the safety of sotalol, and (3) predictors of sotalol efficacy. Thirty-three patients, 28 with paroxysmal and five with chronic atrial fibrillation or atrial flutter, received an average dose of 265 +/- 119 mg of oral sotalol per day. During a 10 +/- 12 month follow-up, recurrence rate for paroxysmal arrhythmia was 64%, with a 50% recurrence at 4.6 months. For patients with chronic atrial fibrillation, ventricular rates were well controlled with sotalol administration (136 +/- 33 beats/min versus 88 +/- 23 beats/min; p = 0.04). No patient with chronic atrial fibrillation converted to sinus rhythm during the study. Side effects necessitated sotalol discontinuation in three patients. By multivariate analysis, younger age, higher ejection fraction, and absence of hypertension independently predicted sotalol efficacy.

Lead fracture in cephalic versus subclavian approach with transvenous implantable cardioverter defibrillator systems.

Lead fracture, occurring in approximately 1%-4% of patients, is an infrequent, but potentially catastrophic complication of permanent pacing systems. Its incidence in transvenous defibrillator systems has not been established. We analyzed data from 757 patients undergoing implantation of transvenous cardioverter defibrillator systems using the Medtronic Transvene Lead system between October 20, 1989 and June 25, 1992 to determine if site of venous approach influenced incidence of lead fracture. All patients received a 3-lead system in 1 of 3 configurations: (1) right ventricle/superior vena cava/subcutaneous patch; (2) right ventricle/coronary sinus/subcutaneous patch; or (3) right ventricle/superior vena cava/coronary sinus. Of 767 right ventricular leads placed, 523 were placed via the subclavian vein, 221 via cephalic vein, and 18 via the internal jugular (5 leads were implanted using another vein). The total number of leads is greater than the total number of patients, as five patients received a second defibrillator system if the initial system was explanted and reimplanted for any reason. Seven patients (0.9%) had right ventricular lead fracture, presenting with inappropriate defibrillator shocks (1), loss of pacing ability (3), both loss of pacing ability and inappropriate shocks (1), or increased pacing threshold (2). All patients required reoperation. All had leads placed by the subclavian venous approach, with chest X ray confirming fracture at the clavicle-first rib junction in 6 of 7 cases. Using Fisher's Exact test, the difference in lead fracture between subclavian and cephalic vein implant approached statistical significance (P = 0.08). The trend toward increased lead fracture incidence with leads placed via subclavian vein suggests that cephalic vein approach may be preferable to avoid this complication.

Simultaneous assessment of myocardial perfusion and left ventricular function during transient coronary occlusion.

OBJECTIVES: We used technetium-99m sestamibi imaging to evaluate the magnitude of changes in left ventricular function and perfusion and to investigate their interdependence during transient coronary occlusion. BACKGROUND: Transient coronary occlusion during coronary angioplasty provides a unique opportunity for examining the effects of acute myocardial ischemia on left ventricular function and perfusion. METHODS: Thirty-five patients with normal left ventricular function underwent first-pass radionuclide angiography with technetium-99m sestamibi using a multicrystal gamma camera during balloon occlusion of a coronary artery. Single-photon tomography was performed 2.1 +/- 1.7 h later. Subsequently, all scans were repeated at rest. RESULTS: The mean size +/- SD of the perfusion defect during coronary occlusion was 23 +/- 18%, with significantly larger defects observed for occlusions of the left anterior descending coronary artery (39 +/- 20%) than for occlusions of the left circumflex (15 +/- 11%) or right (15 +/- 9%) coronary artery (p < 0.05). The mean change in ejection fraction from recovery to occlusion was -17 +/- 17% and was significantly larger for left anterior descending (-26 +/- 21%) and left circumflex (-15 +/- 11%) than for right (-8 +/- 10%) coronary artery occlusions (p < 0.05). For the entire group, ejection fraction during occlusion correlated significantly with perfusion defect size (r = 0.63, p = 0.0004), whereas the extent of ischemic myocardium correlated with the decrease in ejection fraction (r = 0.69, p = 0.0001). The defects present during occlusion reversed within a few hours. CONCLUSIONS: Changes in left ventricular function and perfusion develop pari passu during coronary occlusion and are more severe when the left anterior descending artery is occluded. Although a significant correlation exists between the extent of the perfusion defect and the severity of the decrease in ejection fraction, there is a substantial individual variation with respect to changes in both myocardial perfusion and ventricular function during acute coronary occlusion.

Comparison of ventricular function in atrial rate adaptive versus dual chamber rate adaptive pacing during exercise.

The hemodynamic effects of two different pacing modes--rate adaptive atrial (AAIR) versus dual chamber (DDDR) pacing--were assessed in 12 patients with DDDR pacemakers during upright bicycle exercise first-pass radionuclide angiography using a multiwire gamma camera with tantalum-178 as a tracer. All patients had sinus node disease with intact AV conduction. Patients exercised to the same heart rate in random order in these two different pacing modes, AAIR and DDDR with AV delay (of 100 msec) selected to maintain 100% ventricular capture. Cardiac output increased significantly above baseline values during exercise in both pacing modes: 154 +/- 41% (mean +/- SEM, P = 0.002) with AAIR, versus 95 +/- 24% (P = 0.004) with DDDR (P = NS between the two modes). The peak filling rate, likewise, increased in both pacing modes (2.3 +/- 0.21 end-diastolic volumes/sec to 3.8 +/- 0.31 end-diastolic volumes/sec in AAIR [P = 0.0004] and 2.2 +/- 0.18 end-diastolic volumes/sec to 3.4 +/- 0.27 end-diastolic volumes/sec in DDDR [P = 0.0008]). LV ejection fraction was normal at rest (60 +/- 4%, SEM) and did not significantly change with submaximal exercise in either pacing mode (both 56%, P = NS). No significant changes in end-diastolic volume or stroke volume indexes occurred with exercise in either pacing mode. Our study demonstrates that in patients with normal resting LV function, AAIR and DDDR pacing are equally effective in attaining appropriate increases in cardiac output and LV filling during exercise.

Therapeutic significance of exercise-induced ST-segment elevation in patients without previous myocardial infarction.

Twelve patients with exercise-induced ST-segment elevation without prior myocardial infarction, electrocardiographic evidence of left ventricular hypertrophy or left bundle branch block underwent thallium-201 tomography immediately after exercise and 4 hours later. Coronary angiography and left ventriculography were performed within an average of 8 days of exercise testing. Five patients had repeat exercise thallium-201 tomography after medical therapy or revascularization. All patients had large, reversible perfusion defects (average defect size 33.5 +/- 13%), with 11 of 12 patients having a > or = 25% stress perfusion defect. In 10 patients with atherosclerotic coronary artery disease, the average stenosis of the involved vessel was 93 +/- 9% (range 70 to 100). The electrocardiographic leads with ST-segment elevation predicted the site of reversible hypoperfusion. Two patients had extensive, reversible anterior hypoperfusion due to exercise-induced spasm of minimally stenosed left anterior descending coronary arteries. Follow-up exercise testing in 5 patients showed abolition of reversible hypoperfusion and ST changes after medical therapy or revascularization. In patients without prior myocardial infarction, exercise-induced ST-segment elevation signifies extensive, reversible hypoperfusion that can be abolished by revascularization in patients with critical coronary stenoses and by medical therapy in those with coronary vasospasm.