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Biomedical subjects

M B Simson

Publications and source records attributed to M B Simson.

At least 37 records · Page 2Linked to original sources
PubMed1985

Relation of late potentials to site of origin of ventricular tachycardia associated with coronary heart disease.

Signal-averaged electrocardiograms and endocardial catheter mapping were performed in 41 patients with coronary artery disease and sustained ventricular tachycardia (VT) to determine the relation between signal-averaged late potentials (SA-LPs) and catheter-mapped late activity (CM-LA) to the site of origin of VT. The 41 patients had 79 morphologically distinct VTs. Either CM-LA or SA-LP was present during sinus rhythm in 37 of 41 patients (90%). Twenty-two out of 30 patients (73%) had CM-LA corresponding to SA-LP during normal sinus rhythm. Patients with SA-LP had a significantly greater number of sites of CM-LA, which were later and longer in duration than patients without SA-LP present during sinus rhythm. In a select group of patients, those with both SA-LP and CM-LA, the site of origin of VT was located at or adjacent to a site of CM-LA during sinus rhythm in 38 of 44 (86%); however, 36 of 78 sites (46%) of CM-LA were clearly distant from the site of origin of VT. In conclusion, CM-LA corresponding to SA-LP in patients with VT is sensitive but not specific for the site of origin of VT.

Adult↗
PubMed1985

The effects of premature stimulation of the His bundle on epicardial activation and body surface late potentials in dogs susceptible to sustained ventricular tachyarrhythmias.

Experiments were performed on 20 anesthetized dogs to determine the effects of premature stimulation of the His bundle on epicardial conduction and late potentials recorded on the body surface. Fifteen dogs underwent occlusion of the left anterior descending coronary for 2 hr followed by reperfusion, and five that did not undergo operation served as controls. Animals were studied 2 to 52 weeks after the induction of infarction, and four animals with infarction and four control animals exhibited no sustained arrhythmias in response to programmed ventricular extrastimulation. Five dogs with infarction and one control dog had ventricular fibrillation while the six remaining dogs had inducible sustained ventricular tachycardia. All animals with ventricular tachycardia had late potentials in the terminal portion of the signal-averaged body surface QRS complexes during sinus rhythm and QRS durations in the animals were 64 msec or greater. The voltage in the last 20 msec of the QRS complex was 13.5 microV or less and the duration of late activity below 30 microV was 18.2 msec or more. These values did not overlap values in animals with no inducible arrhythmias. Ventricular fibrillation was a nonspecific end point in these experiments and values overlapped those in animals with no arrhythmias and those with ventricular tachycardia. All animals with infarction and late potentials associated with their QRS complexes also had delayed and prolonged epicardial electrograms that extended into the time of the late potentials recorded from 45 standard sites in the infarcted regions. A single premature beat evoked by His bundle pacing (coupling interval of 192 to 270 msec) had no significant effect on late potentials or their relationship to epicardial activation in the area of infarct. However, changes in the durations of electrograms in response to premature beats were different in animals with infarction and ventricular tachycardia than in those with ventricular fibrillation. In animals with ventricular tachycardia, electrograms at 15 of 210 sites increased in duration by more than 10 msec while those at 61 of 210 sites decreased in duration. In animals with ventricular fibrillation, electrograms at 40 of 207 sites were of increased duration while those at 26 of 207 decreased. The decreases in duration were usually due to components of fractionated electrograms "dropping out" and likely represent local conduction block near the recording electrode.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Abnormal signal-averaged electrocardiograms in patients with nonischemic congestive cardiomyopathy: relationship to sustained ventricular tachyarrhythmias.

We assessed whether signal-averaged electrocardiography could identify patients with sustained ventricular arrhythmias in 41 patients with non-ischemic cardiomyopathy. Twelve of these patients presented with sustained ventricular arrhythmia and 29 patients had no history of sustained ventricular arrhythmias. The mean ejection fractions in the groups were 30 +/- 9% and 24 +/- 9%, respectively. Results were compared with signal-averaged electrocardiograms in 55 normal individuals. The filtered QRS duration was longest in patients with sustained ventricular arrhythmias (130.2 +/- 19.5 vs 105.0 +/- 13.1 msec in the group without sustained ventricular arrhythmia, p less than .001 and 95.9 +/- 9.1 in the normal group, p less than .001). The voltage in the last 40 msec of the filtered QRS was lower in the sustained ventricular arrhythmia group (11.3 +/- 9.3 microV) than the group without sustained ventricular arrhythmia (53.5 +/- 28.3 microV; p less than .001) or the normal group (53.7 +/- 25.2 microV; p less than .001). Eighty-three percent of patients in the sustained ventricular arrhythmia group had an abnormal signal-averaged electrocardiogram characterized by both a long filtered QRS duration and a late potential of low voltage level; only 2% of normal subjects and 14% of patients without sustained ventricular arrhythmias had an abnormal signal-averaged electrocardiogram. The signal-averaged electrocardiogram can identify patients with nonischemic congestive cardiomyopathy and sustained ventricular arrhythmias.

Adult↗
PubMed1985

Recovery of left ventricular function after graded cardiac ischemia as predicted by myocardial P-31 nuclear magnetic resonance.

The purpose of this study was to determine noninvasively some critical level of high-energy phosphate stores that relates to the recovery of ventricular contractile function after graded cardiac ischemia. Rabbit hearts (n = 30) were equipped with an intraventricular balloon to monitor developed pressure and +/- dp/dt and placed in a nuclear magnetic resonance magnet (Bruker, 4.7 Tesla). Each heart underwent 10, 20, 40, or 60 minutes of global ischemia followed by 1 hour of reperfusion. The pH as determined by nuclear magnetic resonance dropped from 7.14 +/- 0.04 to 7.07 +/- 0.07 (p less than 0.02) at 1 minute and to 6.19 +/- 0.08 at 30 minutes of ischemia; pH ceased to fall thereafter. Phosphocreatine was depleted to 10% +/- 7% of its preischemic control in 10 minutes. Adenosine triphosphate (ATP) concentrations were 71% +/- 14% and 1% +/- 2% at 10 and 60 minutes. Regression analysis of recovered developed pressure on end-ischemic ATP (EIATP) revealed: developed pressure = 0.93 (EIATP) + 23 (r2 = 0.99). We conclude that: anaerobic metabolism as evidenced by a fall in pH appears to be active for 30 minutes after normothermic ischemia and then ceases; phosphocreatine buffers the fall in ATP during early ischemia; there is a tight correlation between EIATP and recovery of left ventricular contractile function with a threshold content of approximately 80% below which recovery of function will not be complete.

Adenosine Triphosphate↗
PubMed1984

Identification of patients with ventricular tachycardia after myocardial infarction: signal-averaged electrocardiogram, Holter monitoring, and cardiac catheterization.

Electrocardiographic signal averaging techniques have demonstrated a low-amplitude late potential and a long filtered QRS complex in patients with ventricular tachycardia (VT) after myocardial infarction. Complex ventricular ectopy and left ventricular aneurysms have also been associated with VT. The purposes of this study were (1) to determine whether the findings from the signal-averaged electrocardiogram (ECG) were independent of those from Holter monitoring and cardiac catheterization and (2) to determine the combination of findings from the signal-averaged ECG, cardiac catheterization, and Holter monitoring that best characterize patients with VT after myocardial infarction. We studied 174 patients after myocardial infarction, 98 of whom had recurrent sustained VT. By multivariate logistic regression only three parameters were found to be independently significant, listed in order of power: positive signal-averaged ECG (presence of a late potential or a long filtered QRS duration), peak premature ventricular contraction greater than 100/hr, and presence of a left ventricular aneurysm (p less than .001). The signal-averaged ECG provides independent information in identifying patients with VT after myocardial infarction.

Adolescent↗
PubMed1984

Body surface late potentials: effects of endocardial resection in patients with ventricular tachycardia.

We studied 37 patients undergoing endocardial resection for medically refractory ventricular tachycardia (VT). Each was studied before and after surgery by programmed ventricular stimulation and signal-averaged electrocardiography. Low-amplitude late potentials were identified preoperatively in 76% of patients. In the 24 patients without postoperative VT the effect of surgery was to shorten the filtered QRS duration (137 +/- 27 to 121 +/- 26 msec; p = .003), increase the voltage in the last 40 msec of the filtered QRS (16.5 +/- 16.1 to 39.0 +/- 29.4 microV; p = .003), and decrease the incidence of late potentials (71% to 33%; p = .03). The filtered QRS complex was unchanged in 13 patients whose VT persisted after surgery. No preoperative variable predicted which patients would not have inducible VT after surgery. However, loss of a late potential after surgery in nine of 10 patients was associated with absence of inducible VT (p less than .02). Loss of a late potential was not necessary for surgical success. Eight of 18 patients with a persistent late potential did not have inducible VT. The signal-averaged electrocardiogram predicted a successful outcome after endocardial resection if the late potential was no longer present.

Cardiac Pacing, Artificial↗
PubMed1984

Heart transplant rejection monitored by signal-averaged electrocardiography in patients receiving cyclosporine.

Data from standard and high-frequency signal-averaged electrocardiograms (ECGs) were correlated with the results of 67 endomyocardial biopsies performed in 20 cyclosporine-treated heart transplant recipients. Eight patients (group 1) were in the early postoperative hospitalization period and 12 patients (group 2) were studied after their hospital discharge. The biopsy samples were classified as normal or as indicating early (cellular infiltrate) or definite rejection (myocyte necrosis). The standard ECG parameter studied was the summated QRS voltage in leads I, II, III, V1, and V6. The signal-averaged ECG was evaluated for QRS duration, high-frequency voltage amplitude of the total QRS complex and of its three thirds, peak QRS voltage amplitude, and QRS integrated voltage-time product. The ECG recording obtained at the time of a first normal biopsy sample was considered the normal reference to which additional tracings from the same patient were compared. At the time of subsequent biopsies, the standard ECG parameter showed poor reproducibility (r = .58) and it was inadequate in defining rejection episodes in the early or late postoperative period. The signal-averaged ECG was more reproducible (r = .83) and more accurate in detecting definite rejection during the late posttransplant period than the standard ECG. In group 2 patients, 92% of abnormal signal-averaged ECG recordings were associated with rejection episodes and only 13% of normal tracings were associated with definite rejection. The method was inadequate, however, in monitoring patients during the early postoperative period and in detecting mild forms of rejection in the late postoperative phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Relation between late potentials on the body surface and directly recorded fragmented electrograms in patients with ventricular tachycardia.

The relation between low-amplitude, late potentials on the body surface and directly recorded electrograms in 8 patients with and 11 patients without ventricular tachycardia (VT) was studied. Bipolar X,Y,Z leads were signal-averaged and filtered with a digital technique. All patients had catheter endocardial left ventricular maps. The VT group had medically intractable VT and an endocardial excision was performed for control of VT. Before bypass, epicardial maps were obtained in the operating room. All studies were performed during normal sinus rhythm. Four patients without VT, each with a previous myocardial infarction, had fragmented endocardial electrograms recorded at 2.0 +/- 1.2 sites. The latest electrogram for each patient ended 87 +/- 8 ms after QRS onset, within the high-amplitude portion of the filtered QRS complex. All patients with VT had fragmented electrograms recorded at 6.1 +/- 3.1 sites/patient. Eighty-eight percent of the fragmented electrograms were endocardial. The latest fragmented electrogram for each patient ended 161 +/- 43 ms after QRS onset, significantly later than the fragmented electrograms from the patients without VT (p = 0.002). Six VT patients had low-amplitude, late potentials at the end of the filtered QRS complex. In these patients, the last 40 ms of the filtered QRS complex contained a higher proportion of fragmented electrograms compared with earlier segments of the QRS complex (68% versus 27%, p less than 0.001). Two patients with VT did not have late potentials. One patient with left bundle branch block had delayed left ventricular epicardial activation which masked the fragmented electrograms. The other had fragmented electrograms of brief duration which ended 80 +/- 12 ms after QRS onset, during the time of normal ventricular activation. It is concluded that the late potential corresponds to delayed, fragmented electrographic activity. Failure to record a late potential may arise from delayed ventricular activation at other sites from bundle branch block or fragmented electrograms of a brief duration.

Adolescent↗
PubMed1983

Right ventricular tachycardia: clinical and electrophysiologic characteristics.

This report describes the clinical and electrophysiologic characteristics of 30 patients without myocardial disease who had ventricular tachycardia with the morphologic characteristics of left bundle branch block and inferior axis. The tachycardias were nonsustained in 24 patients, sustained (greater than 30 sec) in six patients, and provocable by exercise in 14 of 23 patients undergoing a standard Bruce protocol. Ventricular tachycardia was induced during electrophysiologic study in 22 of 30 patients. Programmed stimulation induced tachycardia in 10 of 30 patients, most frequently by rapid atrial or ventricular pacing. Isoproterenol infusion facilitated tachycardia induction in 13 of 23 patients. Endocardial activation mapping, performed in 10 patients, confirmed that earliest ventricular activation during tachycardia occurred at the right ventricular outflow tract on the interventricular septum. These tachycardias were unique in their responsiveness to a wide variety of antiarrhythmic drugs, including type I drugs and propranolol. During a mean follow-up of 30 months, no patient has died or experienced cardiac arrest. Two patients appear to be in spontaneous remission, and no patient has developed additional signs of cardiac disease.

Adolescent↗
PubMed1983

Clinical application of signal averaging.

The signal averaging technique is used to reduce the level of noise contaminating the recording of a periodic signal like the electrocardiogram. The detection of ventricular late potentials and the surface activity of the His bundle and sinus node, as recorded by this technique, are discussed in this article.

Anti-Arrhythmia Agents↗
PubMed1982

Mechanism of action of hyaluronidase in decreasing myocardial ischemia post coronary occlusion in the isolated perfused rabbit heart.

The influence of hyaluronidase (H) on subacute experimental myocardial ischemia was studied in isolated perfused rabbit hearts. Changes in ischemic area were assessed by epicardial nicotinamide adenine dinucleotide (NADH) fluorescence photography, an intrinsic high-resolution display of myocardial ischemia. Computerized determination of ischemic area was made from standardized photographs. Hyaluronidase was begun 20 minutes after coronary artery occlusion at 4 units/ml perfusate. NADH fluorophotographs were taken at 10-minute intervals up to 60 minutes of ischemia. Coronary sinus oxygen tension (PcsO2), myocardial oxygen consumption (MVO2), and coronary flow were determined. After 70 minutes, the hearts were perfused with rhodamine solution to identify areas of myocardial perfusion. In 13 H-treated hearts 54.3% +/- 3.7% (mean +/- SEM) of the nonperfused area (rhodamine stained) was ischemic (NADH fluorescent). In 14 untreated hearts 79.8% +/- 3.2% of the nonperfused area was ischemic (p less than 0.0001) and the ischemic areas were uniform. The distance between perfused and ischemic tissue was 952 +/- 78 micrometers in the H hearts and 504 +/- 35 micrometers in the untreated heart (p less than 0.0001). In the H hearts PcsO2 increased to 155% of the post-ligation control while it decreased to 79% in the untreated hearts (p less than 0.0001). MVO2 decreased in the H-treated hearts to 62%; the untreated hearts had no further change. In the H-treated hearts, coronary flow increased to 146% of the post-ligation control while it fell to 91% in the untreated group (p less than 0.0001). We conclude that H increases coronary flow while decreasing MVO2 during subacute ischemia. In H-treated hearts, significant amounts of myocardium remain normoxic within the nonperfused areas, and may potentially be salvaged after prolonged myocardial ischemia.

Animals↗
PubMed1982

Pharmacologic modification of myocardial ischemia.

The value of three agents in reducing the area of myocardial ischemia in rabbit hearts perfused with crystalloid solution was examined. Ten hearts received crystalloid solution with methylprednisolone (M), 0.25 mg/ml; 18 with hyaluronidase (H), 4 U/ml; and 10 with propranolol (P), 1 microgram/ml. Thirty-six hearts served as controls. The mitral valves were excised, the hearts were paced at 240 beats/min and a coronary artery was ligated. The ischemic area was evaluated by nicotinamide adenine dinucleotide autofluorescence photography, an intrinsic, high-resolution display of anoxic tissue. The ischemic area was determined by computer from standardized photographs. Myocardial oxygen consumption (MVO2) was determined and photographs were taken before and at 10-minute intervals after ligation. At 60 minutes, each heart was perfused with rhodamine dye and quick-frozen. In hearts treated with M and H, coronary blood flow increased by 151% (51.7 +/- 3 to 77.9 +/- 3 ml/min) and 150% (48.3 +/- 2 to 72.3 +/- 2 ml/min), respectively (p less than 0.001), whereas in hearts treated with U and P, coronary flow decreased at 60 minutes. In the control hearts, the ischemic area did not change between 5 and 40 minutes of ischemia. The ischemic area of H-treated hearts decreased from 136 +/- 4 mm2 to 110 +/- 9 mm2 between the postligation control and the end of the experiment (p less than 0.01). The ischemic area of M-treated hearts decreased from 131 +/- 5 mm2 to 113 +/- 5 mm2 (p less than 0.05). P produced no change in ischemic area (p greater than 0.4). There was no change in the oxygen-diffusion zone of P-treated or control hearts (439 +/- 13 vs 383 +/- 12 mu, p greater than 0.1). The oxygen-diffusion zone between perfused and anoxic tissue in the M and H hearts increased from 383 +/- 12 mu to 861 +/- 76 mu and 681 +/- 62 mu, respectively (p less than 0.001). We conclude that significant volumes of myocardium remain normoxic within nonperfused areas of M-, P- and H-treated hearts.

Animals↗
PubMed1982

The incidence and clinical significance of epicardial late potentials in patients with recurrent sustained ventricular tachycardia and coronary artery disease.

Seventy-eight patients with ventricular tachycardia associated with coronary artery disease underwent intraoperative mapping while in sinus rhythm to evaluate the frequency and significant of late potentials. In 30 of these patients, the surface ECG was subjected to signal averaging to correlate the incidence and duration of low-amplitude, delayed electrograms with the presence of late potentials recorded during epicardial mapping. One to four epicardial late potentials were observed in nine patients (11.5%). These nine patients did not differ hemodynamically from patients without late potentials. In four patients, the site of epicardial breakthrough during ventricular tachycardia bore no relationship (i.e., greater than 3 cm away) to the late potential or the site of origin of the tachycardia. In the five other patients with late potentials, epicardial breakthrough and site of origin of ventricular tachycardia were closely related to the free wall of an apical aneurysm. However, three of these patients had additional tachycardias from disparate sites. Twenty-seven of 30 patients in whom signal averaging was used had a low-amplitude signal in the terminal 40 msec of the amplified QRS complex. In 24 of these 27 patients (89%), the low-amplitude tail was demonstrated in the absence of epicardial late potentials. We conclude that epicardial late potentials are found infrequently in patients with ventricular tachycardia associated with coronary artery disease; epicardial late potentials cannot be used to localize ventricular tachycardia; and the specific low-amplitude tail on the signal-averaged electrogram is unrelated to epicardial events.

Adult↗
PubMed1982

Initiation of ventricular tachyarrhythmia with programmed stimulation: sensitivity and specificity in an experimental canine model.

Programmed stimulation (PS) is used in the catheterization laboratory and operating room to initiate and study malignant ventricular tachyarrhythmia (VT). The purpose of this study was to evaluate the specificity and sensitivity of PS in short-term studies of 10 normal animals (group A), 10 sham-operated controls (group B), and 10 dogs with chronic myocardial infarction susceptible to inducible VT by an occlusion-reperfusion method (group C). Groups B and C were studied 7 to 14 days after the initial procedure. the pH, PaO2, and PaCO2 were determined and corrected every 30 minutes during the procedure. When bipolar ventricular pacing with three ventricular extrastimuli was used, VT initiation was attempted at 10 normal intramyocardial sites in groups A and B and in close proximity (less than or equal to 1 cm) to areas of infarction in group C. When one ventricular extrastimulus was used during ventricular pacing, VT was induced in dogs with chronic infarctions (3 of 10, 30%, group C). Using two extrastimuli, however, VT was inducible in 4 of 10 (40%) of group A, 6 of 10 60%) of group B, and all 10 (100%) of group C. With three extrastimuli, all 30 dogs had inducible VT. Overall, PS with one extrastimulus was highly specific in 100% but insensitive in 30%. With two extrastimuli the sensitivity increased to 100%, but the specificity fell to 50%. Finally, with three extrastimuli the sensitivity was also 100%, but the specificity decreased to 0%. PS remains an invaluable technique in diagnosing and assessing therapy for patients with VT. The diagnostic implications of this test await more precise pathophysiologic elucidation of arrhythmic mechanisms.

Animals↗
PubMed1981

Stability of an experimental atrioventricular reentrant tachycardia in dogs.

The factors leading to spontaneous block and instability of a reentrant tachycardia were studied with a computer model and in eight anesthetized dogs with an electronically simulated atrioventricular (AV) bypass tract. The bypass tract delay could be changed in a programmed sequence. AV nodal refractoriness in the dogs was increased with verapamil. Stability of the reentrant tachycardia was assessed by noting how rapidly cycle-length changes from a transient alteration in the bypass-tract delay time would dampen out and the tendency of the reentrant tachycardia to spontaneously block. There was close agreement between computer model predictions and experimental results. After a transient change in bypass tract delay time, dampened oscillations of the cycle length were noted. The degree of dampening was related to the slope of the AV nodal refractory curve. When the reentrant tachycardia operated on a steep portion of the refractory curve (slope steeper than -1), spontaneous oscillations and block developed. In the dog, the reentrant tachycardias terminated spontaneously either by an increase in amplitude of oscillations or by an increase in AV nodal refractoriness. We conclude that, for stable reentry, a reentrant circuit must have no conduction block and must be able to dampen out transient perturbations.

Animals↗