Harvey L. Waxman

Left ventricular mass regression after aortic valve replacement measured by ultrafast computed tomography

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.

Improvement in early diastolic filling dynamics after aortic valve replacement

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.

Oral amiodarone loading for the rapid treatment of frequent, refractory, sustained ventricular arrhythmias associated with coronary artery disease

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.

Frequency of low-grade residual coronary stenosis after thrombolysis during acute myocardial infarction

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)

Pacemaker‐Mediated Tachycardia from a Single Chamber Temperature Sensitive Pacemaker

VOLOSIN, KJ. et al.: Pacemaker‐Mediated Tachycardia from a Single Chamber Temperature Sensitive Pacemaker 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 lo sustained upper rate limit pacing. Decreasing the ventricular output to prevent diaphragmatic capture eliminated further episodes of pacemaker‐mediated tachycardia.

Combined ambulatory electroencephalographic and electrocardiographic recordings for evaluation of syncope

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.

Signal‐Averaged ECG Prior to and Serially After Thrombolytic Therapy for Acute Myocardial Infarction

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 μV and 58.6 ± 44.7 μV vs 44.4 ± 35.5 μV, 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.

Differentiation of arrhythmias by measurement of intracardiac pressures in man.

Antitachycardia devices currency 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 atria] 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.

VOOR—Nondemand Rate Modulated Pacing Necessitated by Myopotential Inhibition

This report describes the use of the temperature sensitive rate modulated nondemand pacing mode (VOOR) in a patient with significant myopotential inhibition of pacemaker output during exercise. The VOOR mode eliminated myopotential sensing which had prevented an exertion related increase in heart rate. The patient has done well with VOOH pacing for the past year. VOOR pacing is useful in selected cases.

Effects of Exercise on Signal‐Averaged Electrocardiogram

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.