Left ventricular rupture complicating percutaneous mitral commissurotomy: salvage using percutaneous cardiopulmonary bypass support.

Left ventricular rupture resulting in death has been reported to be a complication of percutaneous mitral commissurotomy. We report a 71-year-old man in whom a left ventricular rupture occurred during percutaneous mitral commissurotomy and resulted in hemodynamic collapse due to acute cardiac tamponade. The patient was stabilized using percutaneously instituted cardiopulmonary bypass support with subsequent repair of the left ventricle and successful mitral valve replacement. Three months later this patient remains in New York Heart Class I.

Percutaneous cardiopulmonary bypass support in the catheterization laboratory: technique and complications.

A safe and easily applied technique of percutaneous cardiopulmonary bypass support has been developed for use in the cardiac catheterization laboratory. The importance of this technique lies in its ability to maintain hemodynamic stability during high risk interventional procedures regardless of intrinsic cardiac function. Venous and arterial cannulas (18F) are inserted percutaneously over a stiff guide wire after sequential dilatation with 12F and 14F dilators. Bypass flow rates of up to 5 L/min can be achieved. This technique can be applied to support patients with cardiac arrest, hemodynamic collapse after abrupt closure during coronary angioplasty, and cardiogenic shock, as well as those undergoing high-risk elective coronary angioplasty. This form of support also permits transport of the patient to the operating room in a stable condition after an unsuccessful angioplasty. The complications are mostly related to cannula removal and can be minimized by the use of a proper technique. Although the ultimate role of this new technique remains to be completely defined, it appears that it will expand the patient population for whom coronary interventions can be applied.

Emergency cardiopulmonary bypass support in patients with cardiac arrest in the catheterization laboratory.

Cardiac arrest in the catheterization laboratory is fatal if unresponsive to advanced cardiac life support (ACLS). Seven patients not responding to ACLS following cardiac arrest in the catheterization laboratory underwent percutaneously instituted cardiopulmonary bypass support. Cardiac arrest occurred following abrupt closure postcoronary angioplasty in three patients, during cardiogenic shock in three patients, and during diagnostic angiography in one patient. Cardiopulmonary bypass was instituted 10-45 min (mean, 21 min) following the onset of cardiac arrest. Flows on bypass ranged from 4.0 to 5.2 liter/min. Mean blood pressure ranged from 70 to 110 mm Hg on bypass. Six of the seven patients regained consciousness after the institution of bypass. Acid-base balance was normalized in all patients. Coronary bypass surgery was subsequently performed in three patients and coronary angioplasty in two. Four patients survived. One patient died following coronary bypass surgery. Two patients, who were not suitable candidates for revascularization, expired. Total bypass time was 1.5-8.5 hr (mean, 2.7 hr). At a mean follow-up of 6 months, all four survivors are alive and asymptomatic or NYHA class 1. We conclude that cardiopulmonary bypass support 1) can stabilize patients following cardiac arrest in the catheterization laboratory, 2) can facilitate emergency coronary angioplasty or transfer to the operating room for coronary bypass surgery, and (3) can improve survival in patients unresponsive to ACLS when instituted early following cardiac arrest in the catheterization laboratory.

The use and interaction of permanent pacemakers and the automatic implantable cardioverter defibrillator.

The adverse interactions of permanent pacemakers and automatic implantable cardioverter defibrillators (AICD) were studied in nine patients in whom both devices were implanted. Both unipolar and bipolar pacemakers were evaluated. The permanent pacemakers were also used to do noninvasive electrophysiological studies and to induce ventricular fibrillation. Undersensing of ventricular fibrillation by the permanent pacemakers caused inappropriate pacemaker stimuli, which caused undersensing of ventricular fibrillation by the AICD in three of four patients with unipolar pacemakers. After an AICD discharge, pacemaker noncapture was seen in eight of 22 episodes for an average 4.9 seconds and inability to sense was seen in 11 of 20 episodes for an average 9.0 seconds. Counting of pacemaker stimuli and QRS by the AICD caused inappropriate discharges. Noninvasive electrophysiological testing by the pacemakers correlated with invasive testing. Furthermore, induction of ventricular fibrillation was successful in four of five patients attempted, though requiring long bursts at high outputs at the shortest cycle lengths obtainable by these pacemakers. Operation of the AICD and permanent pacemakers must be clearly understood to avoid adverse interactions of these devices.

Noninvasive electrophysiologic study using standard permanent pacemakers in patients with spontaneous sustained ventricular tachycardia or ventricular fibrillation.

Permanent pacemakers capable of noninvasive electrophysiologic testing were used to study and treat 26 patients with spontaneous sustained ventricular tachycardia (VT) or fibrillation (VF). One hundred nine episodes of sustained VT or VF were induced in these patients. In 8 patients spontaneous VT was reverted by noninvasive means. Drug changes based on noninvasive testing were made in 12 patients. In the 1- to 67-month follow-up period, drug therapy based on noninvasive electrophysiologic testing was predictive of outcome in patients with spontaneous arrhythmias. Thus, noninvasive electrophysiologic testing using permanent pacemakers is a useful method for studying and treating patients with recurrent sustained ventricular arrhythmias.

Reduced acetylation of procainamide by para-aminobenzoic acid.

Acetylation is the major route of metabolism of many drugs including the antiarrhythmic agent procainamide. Coadministration of para-aminobenzoic acid was observed to decrease the biotransformation of procainamide to N-acetylprocainamide in a patient with rapid acetylation kinetics. In view of the distinct antiarrhythmic and toxic properties of procainamide and N-acetylprocainamide, the observed drug interference may have great clinical relevance in long-term oral antiarrhythmic therapy and in instances where other drugs converge for acetylation.