A model of chronic ischemic arrhythmias: the relation between electrically inducible ventricular tachycardia, ventricular fibrillation threshold and myocardial infarct size.

To study the relation between inducible ventricular tachycardia and ventricular vulnerability, myocardial infarction was created in 22 closed chest mongrel dogs by inflating a balloon catheter in the left anterior descending coronary artery for 2 hours. The presence of inducible ventricular tachycardia was determined by programmed electrical stimulation of the right ventricle in each dog before and 4 days after infarction, using a transvenous electrode catheter and a "clinical" stimulation protocol. In each dog the repetitive ventricular response threshold and the ventricular fibrillation threshold were measured before and 4 days after infarction. Ventricular tachycardia was not inducible in any dog before infarction. After infarction, sustained ventricular tachycardia was inducible in 10 (45 percent) of 22 dogs and nonsustained tachycardia in an additional 4 dogs (18 percent). Ventricular fibrillation threshold was greatly reduced 4 days after infarction in dogs with inducible sustained tachycardia (mean +/- standard deviation 29 +/- 11 to 10 +/- 5 mA, p less than 0.001); the mean threshold did not change significantly in dogs without inducible sustained tachycardia. Both the ventricular fibrillation threshold and mean ventricular repetitive response threshold were reduced in the dogs with sustained ventricular tachycardia; neither was significantly altered in the dogs without sustained tachycardia. The magnitude of change in the two thresholds frequently differed; hence, a correlation was weak between the control and postinfarction repetitive response/fibrillation threshold ratio (r = 0.41). Postmortem measurement of infarct size demonstrated an association between this measurement and the presence of inducible ventricular tachycardia. Sustained ventricular tachycardia was not inducible in the presence of a small infarct. It is concluded that: (1) inducible ventricular tachycardia on the 4th day after myocardial infarction is associated with a considerable decrease in the ventricular fibrillation threshold; (2) changes in the repetitive response and fibrillation thresholds after myocardial infarction may not be parallel, complicating the use of the repetitive ventricular response threshold as a substitute for the ventricular fibrillation threshold in the postinfarction state; (3) a large infarct predisposes the heart to electrically inducible sustained ventricular tachycardia.

Response to programmed ventricular stimulation: sensitivity, specificity and relation to heart disease.

This prospective study of 100 patients evaluated the sensitivity and specificity of the repetitive ventricular response and ventricular tachycardia induced by programmed electrical stimulation for identifying patients with spontaneous ventricular tachyarrhythmias. The influence of underlying heart disease on such sensitivity and specificity was also evaluated. The repetitive ventricular response was sensitive (92 percent) for detecting patients with prior spontaneous ventricular tachyarrhythmias, but lacked specificity (57 percent); the rate of false positive responses was 43 percent. Inducible ventricular tachycardia was less sensitive (65 percent) but more specific (98 percent); the rate of false positive responses was only 3 percent. Among the 100 patients, 71 had heart disease, 29 did not. The presence of underlying heart disease had no significant effect on the sensitivity and specificity of repetitive ventricular responses or ventricular tachycardia induced by programmed stimulation; it did not increase the rate of false positive responses. It is concluded that (1) ventricular tachycardia induced with programmed ventricular stimulation is an excellent basis for guiding the management of clinically significant ventricular tachyarrhythmias, regardless of underlying heart disease; and (2) the repetitive ventricular response is not useful for this purpose because of its high rate of false positive responses among patients with or without significant heart disease.

Effect of electrophysiological testing on ejection fraction during cardioverter/defibrillator implantation.

To evaluate the effect of repeated induction of ventricular tachycardia or ventricular fibrillation, or both, in patients with poor left ventricular function, we performed intraoperative two-dimensional echocardiography in 6 patients undergoing implantation of the automatic implantable cardioverter/defibrillator. Changes in left ventricular ejection fraction in sinus rhythm were assessed before the first inducible ventricular arrhythmia and after a mean of 6 +/- 1.9 (SD) episodes of ventricular tachycardia or ventricular fibrillation. During the procedure no significant change in mean ejection fraction was observed (28 +/- 14 versus 27 +/- 17%). Only 1 of the 6 patients studied had a change in ejection fraction greater than 3% (a decrease from 20 to 11%). In an overall clinical series of 38 primary implants or generator changes (including electrophysiological testing) in 29 patients, 1 patient recovered after postoperative inotropic support and 1 died of acute postoperative ischemic heart failure. We conclude that ventricular arrhythmias induced during automatic implantable cardioverter/defibrillator implantation have no immediate deleterious effects on ejection fraction in most patients with compromised left ventricular function and without ongoing ischemia.

Sinus node recovery times following the spontaneous termination of supraventricular tachycardia and following atrial overdrive pacing: a comparison.

We compared the pauses that followed the spontaneous termination of supraventricular tachyarrhythmias with the pauses that followed the cessation of atrial overdrive pacing in 21 patients. In 10 patients with abnormal sinus node function and in 11 patients with normal sinus node function we recorded the spontaneous termination of supraventricular tachyarrhythmia in the clinical electrophysiology laboratory; a strong correlation (r = 0.94) was found between the maximal spontaneous sinus node recovery time and the maximal paced sinus node recovery time. A weaker correlation was found between the paced and spontaneous sinus node recovery times (r = 0.57) when the spontaneous termination of supraventricular tachyarrhythmia was recorded during ambulatory electrocardiographic recording in seven patients. Spontaneous sinus node recovery times were significantly shorter than maximal paced sinus node recovery times (p less than 0.001). However, no significant difference was detected between the paced and spontaneous sinus node recovery times when atrial pacing was performed at the rate of the tachycardia. We conclude that spontaneous and postpacing sinus node recovery times are closely correlated. The paced sinus node recovery time is, however, frequently more prolonged than spontaneous sinus node recovery time because of probable atriosinus entrance block during rapid supraventricular tachycardia.

Sinus node echoes and concealed concealed conduction: additional sinus node phenomena confirmed in man by direct sinus node electrography.

Direct sinus node electrography has been previously used to assess several aspects of sinus node physiology: sinus node pauses, overdrive suppression, sinoatrial entrance block. This report presents data in which sinus node electrograms confirm two additional physiologic phenomena in man: concealed conduction in the sinoatrial junction and sinus node reentry. These findings verify the presence of previously suspected phenomena by careful deductive analysis of electrocardiographic and electrographic tracings.

Unexplained in-hospital fever following cardiac surgery. Natural history, relationship to postpericardiotomy syndrome, and a prospective study of therapy with indomethacin versus placebo.

In Part I of this study, the in-hospital course of 219 patients who had undergone a cardiac operation is analyzed. Fever (greater than or equal to 37.8 degrees C, rectal) was present after postoperative day 6 in 159 patients (73%) and was of unexplained cause in 118. Fever decay in the population of unexplained fever patients was exponential. All patients with unexplained postoperative fever were afebrile by postoperative day 19. In-hospital pericardial rub and pleuritic chest pain, widening of the mediastinum on chest film, and pleural effusion were not specifically associated with unexplained postoperative fever. In Part II, 67 patients with unexplained postoperative fever were given indomethacin (100 mg per day) or placebo for 7 days by a randomized, double-blind protocol. Indomethacin resulted in a shorter duration of fever (2.4 vs 3.5 days, P is less than 0.01) and in a shorter duration of chest pain, malaise, and myalgias compared to placebo. Sixty-seven percent of the patients in Part I and all of the patients in Part II were contacted 2-8 months following hospital discharge. Five percent had experienced an illness that we considered to be acute pericarditis, but its occurrence was unrelated to whether the patient had had in-hospital unexplained postoperative fever, in-hospital rub or chest pain, or in-hospital administration of indomethacin.