High-grade Ventricular Ectopy Research Articles

The incidence of arrhythmias during exercise stress tests among children with Kawasaki disease: A single-center case series.

Based on 2017 guidelines, participation in competitive sports with prior history of Kawasaki Disease (KD) requires those with coronary artery aneurysms (CAA) z score ≥ 5 to undergo evaluation for evidence of inducible ischemia or arrhythmias. The use of exercise stress testing (EST) to evaluate arrhythmias among KD patients has never been reported. This retrospective single-center case series study sought to describe the presence of inducible arrhythmias during EST in KD patients with or without CAA. Single-center retrospective review of medical records of patients diagnosed with KD between 1989-2015 at Texas Children's Hospital, Houston, Texas who underwent EST were included. Among 1007 patients diagnosed with KD, 95 (9%) underwent 165 ESTs at a median time of 9.6 years (IQR 5.8-11.3 years) from diagnosis. Of these 95 patients, 37 had normal coronaries, 21 dilated (z score 2 to <2.5), 10 small (5 >z ≥2.5), 12 medium (10>z ≥ 5 absolute dimension <8mm), 10 large (z ≥10 or absolute dimension ≥8mm), 5 severe (myocardial infarct or bypass graft). Supraventricular tachycardia was not seen. Ventricular arrhythmias during EST were uncommon and seen only among patients with CAA z ≥5. Ventricular tachycardia occurred in a single patient with a large CAA, known VT and ICD. High-grade ventricular ectopy was seen in one patient who had severe CAA and underwent bypass grafting. Arrhythmias on EST were noted only among patients with CAA z ≥5. The current guidelines are a reasonable approach to increasing healthy activity among KD patients. Clarification regarding which inducible arrhythmias meet criteria for activity restriction may be helpful to guide sport participation.

Follow-Up of Electrocardiographic Findings and Arrhythmias in Patients With Anomalously Arising Left Coronary Artery from the Pulmonary Trunk

Follow-up data and correlation of arrhythmias, electrocardiogram (ECG) changes, and cardiac function in anomalous left coronary artery from the pulmonary trunk or artery have not been previously studied. This is a retrospective single-center review of 44 anomalous left coronary artery from the pulmonary trunk or artery patients diagnosed between 1992 and 2014, at a median age of 3months (3 days to 13years). Clinical history, ECG, Holter, and echocardiogram data were reviewed. ECGs were reviewed for contiguous Q-or T-wave inversions, hypertrophy, bundle branch block, and axis deviation. High-grade ventricular ectopy, supraventricular tachycardia (SVT), and ventricular tachycardia (VT) were recorded. Patients with <6months of clinical follow-up were excluded from longitudinal analysis. At diagnosis, 43 (98%) were noted to have electrocardiographic changes. During hospitalization, arrhythmias were seen in 13 patients (30%): 2 (5%) with sustained VT or ventricular fibrillation, 6 (17%) with high-grade ventricular ectopy, and 4 (9%) with SVT. Seven patients (16%) required antiarrhythmic treatment. During outpatient follow-up, arrhythmias were seen in 11 patients. New arrhythmias were documented in 6 without a history of in-hospital arrhythmias. Of 34 patients with at least 6months follow-up (median 6years, 0.5 to 20years), 20 had left ventricular (LV) dysfunction before surgery. Normalization of function occurred in 94% (median 1year, 5 days to 4years). Electrocardiographic changes persisted in 94% at the time of LV function recovery. In conclusion, electrocardiographic changes and arrhythmias may persist despite recovery of ventricular function. Therefore, prolonged myocardial remodeling may continue even after resolution of LV dysfunction during which time arrhythmias may occur.

Arrhythmias in Adult Patients With Congenital Heart Disease

By the time patients with congenital heart disease (CHD) reach adolescence and early adulthood, rhythm status has often become an active issue, if not the central issue, in their cardiac management. For some, arrhythmias are intrinsic to the structural malformation itself, as is the case with Wolff-Parkinson-White syndrome in the setting of Ebstein’s anomaly, or atrioventricular (AV) block in the setting of “congenitally corrected” transposition of the great arteries (L-TGA). For most other CHD patients, arrhythmias represent an acquired condition related to the unique myocardial substrate created by surgical scars in conjunction with cyanosis and abnormal pressure/volume loads of long duration. This review will attempt to address the major rhythm difficulties faced by adults with CHD, concentrating on electrophysiological features that distinguish CHD from more conventional forms of adult heart disease. A listing of specific arrhythmias and commonly associated congenital defects is provided in Table 1 to serve as an outline for the discussion. View this table: TABLE 1. Specific Arrhythmias and Associated Defects in Adults With Congenital Heart Disease As of 2001, there were estimated to be 800 000 adults with CHD living in the United States,1 a number that has grown steadily as more survivors of childhood surgery reach maturity. Of these, roughly 45% are considered to have mild forms of CHD (eg, atrial septal defect, valvar pulmonary stenosis), 40% are classified as having moderate disease (eg, tetralogy of Fallot, Ebstein’s anomaly), and 15% are considered to have complex disease (eg, single ventricle, transposition of the great arteries). Although arrhythmias can develop within any of the 3 subgroups, the incidence is highest for patients in the moderate and severe categories. Tetralogy of Fallot is an instructive example of moderate CHD with a large arrhythmia burden. As many as one third of patients with repaired tetralogy develop symptomatic atrial tachycardias by …

Exercise-induced cardiac hypertrophy: a substrate for sudden death in athletes?

Cardiac hypertrophy is a general term signifying an increase in cardiac mass in response to applied stress. In mild, early hypertrophy, cardiac myocyte contractile performance may be normal or enhanced, whereas in severe hypertrophy associated with cardiac failure, myocyte contraction is reduced in amplitude and increased in duration. In contrast to the varied contractile response, the duration of electrical excitation shows similar changes in both mild and severe hypertrophy. Action potential duration in mid-myocardial and sub-epicardial layers is increased, which is associated with ventricular arrhythmias (in a similar manner to the long QT syndromes from other causes), based on afterdepolarizations and enhanced automaticity. Single-cell studies following exercise training in animal models show that exercise-induced cardiac hypertrophy displays features similar to mild, compensated hypertrophy from other causes. Developed shortening of unloaded single cells is increased or unchanged, and developed force in single myocytes is enhanced. Action potential duration is increased, apart from in the sub-endocardial layer. As with mild hypertrophy from other causes, this will be pro-arrhythmic because of altered dispersion of repolarization and enhanced automaticity. Major abnormalities of the ECG in man include frequent and complex ventricular ectopy, ST segment changes and prolongation of repolarization. In this review a case is presented for regarding exercise-induced cardiac hypertrophy as being no different from mild cardiac hypertrophy resulting from other, pathological causes. The cellular electrophysiological changes are sufficient to account for many of the abnormalities of the ECG, including high-grade ventricular ectopy. Sudden death in trained athletes who have no evidence of specific heart disease may be a direct consequence of cardiac hypertrophy and altered repolarization.

Magnetic resonance imaging evaluation of cardiac tumor characteristics in infants and children

period. 3 Although most cardiac tumors in pediatric patients are not malignant, they may cause blood flow obstruction, ventricular dysfunction, or arrhythmias that result in significant morbidity and mortality. Rhabdomyoma, which is often associated with tuberous sclerosis, is the most common cardiac tumor diagnosed in children. 3‐6 Its echocardiographic features are well established and additional cardiac imaging tests are seldom required for patient management. 4,5 In contrast, specific imaging characteristics of other childhood cardiac tumors are less well defined. Moreover, treatment strategy varies according to tumor type. For example, a Purkinje cell tumor associated with high-grade ventricular ectopy may require surgical resection, whereas a cardiac hemangioma may be treated with high-dose steroids or interferon. Magnetic resonance imaging (MRI) has been shown to provide useful information on tumor location, boundaries, and tissue characteristics in adults. 7,8 However, only a few studies on MRI evaluation of cardiac tumors include infants and children. 7‐10 Furthermore, little information is available regarding MRI tissue characterization of childhood cardiac tumors. The present study, therefore, reports on the evaluation of 11 infants and children with primary cardiac tumors with an emphasis on correlating MRI tumor characteristics with tissue type.

Evaluation and treatment strategies in patients at high risk of sudden death post myocardial infarction.

Over 50 percent of deaths in patients who survive an acute myocardial infarction are due to fatal ventricular tachyarrhythmias. Patients who survive an episode of sustained ventricular arrhythmia are at highest risk of recurrent cardiac arrest. Electrophysiologic studies have been found to be useful in guiding therapy and reducing mortality in these patients and in patients with syncope due to arrhythmic etiology. Evaluation and treatment of nonsustained ventricular tachycardia post infarction remains somewhat controversial. A recently published trial (MADIT), however, showed improved survival with an implanted defibrillator in patients with coronary disease and asymptomatic nonsustained ventricular tachycardia. Asymptomatic patients post infarction at high risk include those who have significant left ventricular dysfunction, late potentials, high-grade ventricular ectopy, and abnormal heart rate variability. These tests individually, however, have a low positive predictive accuracy. This, combined with the fact that antiarrhythmic drugs are frequently not effective and can be proarrhythmic, leaves the best treatment for these patients uncertain. It is known, however, that beta-adrenoreceptor blocking agents do reduce mortality after an acute myocardial infarction. Early studies have shown mixed results relating to sudden death and total mortality with amiodarone. To date, no other antiarrhythmic drug has shown benefit, while several have been shown to be harmful. Recent studies have also shown some beneficial effects of angiotensin-converting enzyme inhibitors, carvedilol, a third-generation beta-blocking agent with vasodilator properties, and the angiotensin II receptor antagonist losartan. However, their precise role in reducing sudden death needs to be defined further.

Use of electrophysiological studies in the diagnosis and treatment of cardiac patients with left ventricular dysfunction and high grade ventricular ectopy

We studied the sudden death occurrence in 28 patients (23 males, age 59.2 ± 15.6 years) who had a documented cardiac disease with left ventricular dysfunction (ejection fraction ≤ 0.4) and high grade ventricular ectopy. None had suffered from spontaneous sustained ventricular arrhythmia and/or syncope. Their diagnosis and treatment were guided by electrophysiological studies. Electrophysiological studies were performed in the antiarrhythmic drug-free state. In cases when sustained ventricular arrhythmias could be induced, antiarrhythmic treatment was prescribed according to the results of the electrophysiological studies. In cases of non-inducibility, no antiarrhythmic treatment was prescribed. The patients were followed up for a period of 20.6 ± 11.2 months. The end points were occurrence of documented spontaneous sustained ventricular arrhythmia and sudden death. None of the 19 non-inducible patients experienced sudden death or spontaneous sustained ventricular arrhythmia. Two of the nine inducible patients died suddenly ( P = 0.1). The 3-year sudden death mortality rate of the whole group was 7.5%. We conclude that when cardiac patients with high grade ventricular ectopy and left ventricular systolic dysfunction are treated according to the results of electrophysiological studies, it can be expected that their 3-year mortality rate will be low and significantly inferior to that reported for conventionally treated patients.

The role of parasympathetic modulation of the reentrant arrhythmic substrate in the genesis of sustained ventricular tachycardia.

The influence of parasympathetic activity on the reentrant arrhythmic substrate in the genesis of sustained ventricular tachycardia remains unclear. To assess this influence, we studied the heart rate variability in 59 patients referred for invasive electrophysiological testing. In addition, the presence of late potentials and high grade ventricular ectopy, and the left ventricular ejection fraction was determined. The 28 patients with inducible sustained ventricular tachycardia were found to have lower heart rate variability by time- and frequency-domain measurements over 24 hours when compared to the 31 subjects who were noninducible. PNN50 was 4% in the inducible patients, whereas it was 9% in the subjects who were noninducible (P = 0.03). Similarly, HFP24H was 9 and 14 msec, respectively (P = 0.02). MAXHFP1H also differed (20 vs 27 msec [P = 0.04]) but not MINHFP1H (5 vs 6 msec). There was no association between heart rate variability and late potentials, degree of ventricular ectopy, or left ventricular ejection fraction. Thus, vagal tone does not appear to correlate with the presence of late potentials, ventricular ectopy, or left ventricular dysfunction. Low mean as well as maximal vagal tone, in contrast to minimal vagal tone, predicts inducibility of sustained ventricular tachycardia. Our data suggest that the inability to modulate parasympathetic tone appears to be an important determinant in the genesis of reentrant sustained ventricular tachycardia.

Lidocaine prophylaxis in coronary revascularization patients: A randomized, prospective trial

Life-threatening ventricular ectopy can occur after cardiac operations. The actual incidence of ventricular ectopy and the ability to prevent it by the routine prophylactic use of lidocaine hydrochloride have not been established. We performed a double-blind, randomized, prospective trial involving 109 patients undergoing elective coronary artery revascularization. Patients received either lidocaine (n = 54) or a placebo (n = 55) after separation from bypass. A Holter monitor was affixed to each patient for subsequent review, and bedside intensive-care monitors with alarms were used for “real-time” surveillance. The code was broken when potentially malignant ventricular ectopy or side effects attributable to the study drug were noted. Three lidocaine patients and 2 placebo patients were dropped from the study because of hemodynamic instability or bleeding. Of the remaining 104 patients, the code was broken in 12 (24%) of the 51 in the lidocaine group (9 for ectopy and 3 for mental status changes) and 10 (19%) of the 53 in the placebo group (all for ectopy) ( p = not significant). Twenty-four-hour Holter monitor evaluation demonstrated occasional ventricular ectopy in all patients and nonsustained ventricular tachycardia in 28% in the lidocaine group and 48% in the placebo group ( p = not significant). The mean number of runs of ventricular tachycardia per patient was 0.53 in the lidocaine group and 1.6 in the placebo group ( p = 0.035). There were no significant differences in terms of other ventricular ectopy, morbidity, or mortality. No ventricular fibrillation occurred in either group. We conclude that although prophylactic administration of lidocaine may decrease the incidence of nonsustained ventricular tachycardia in patients undergoing routine coronary revascularization, there is no apparent clinical benefit to such a strategy. Lidocaine should be used for treatment of high-grade ventricular ectopy rather than as prophylaxis.

Echocardiographic diagnosis of a mycotic aneurysm of the main pulmonary artery and patent ductus arteriosus

heart block with no evidence of structural heart disease is not necessarily benign and the baby should be observed carefully for the first week or so. High-grade ventricular ectopy could result because of bradycardia and hence such a low heart rate itself is an indication for pacing these newborns. In emergency situations the umblical vein can be successfully utilized for inserting a temporary pacing lead.

What is the best predictor of spontaneous ventricular tachycardia and sudden death after myocardial infarction?

Death during the first year after myocardial infarction is most commonly due to spontaneous ventricular tachycardia (VT) or fibrillation (VF). The purpose of this study was to compare, in a single cohort of patients, the values of inducible VT, delayed ventricular activation, low left ventricular ejection fraction, high-grade ventricular ectopy, and ST segment displacement on exercise in predicting electrical events (witnessed instantaneous death and spontaneous VT or VF) during the first year after myocardial infarction. Three hundred sixty one patients aged less than 71 years underwent electrophysiological study, signal-averaged electrocardiogram, gated blood-pool scan, 24 hour ambulatory electrocardiographic monitoring, and exercise testing 1-2 weeks after myocardial infarction and were then followed up for at least 1 year. There were 34 deaths (eight witnessed instantaneous, 26 other), and nine patients survived one or more episodes of spontaneous VF or VT. Patients with inducible VT were 15.2 times more likely to suffer electrical events than patients without inducible VT. No proportional-hazards model excluding inducible VT was as good a predictor of electrical events as was inducible VT alone. Inducible VT at electrophysiological study was the single best predictor of spontaneous VT and sudden death after myocardial infarction.

Cardiovascular abnormalities in infants prenatally exposed to cocaine

This study utilized a historical cohort to examine the relationship between maternal cocaine use during pregnancy and the occurrence of congenital cardiovascular abnormalities. All neonatal drug screens performed at Boston City Hospital during an 18-month period were reviewed (n = 554); for 214 (39%) screened high-risk neonates, results of toxicologic screens were positive for cocaine, and 340 (61%) neonates had no detectable cocaine. We compared the occurrence of cardiovascular malformations and electrocardiographic abnormalities in these two groups. Matches were sought between these 554 infants and our pediatric cardiology data base, which consisted of inpatient consultation, outpatient consultation, and electrocardiography. Forty-nine patients had drug screens and were also entered into our cardiology data base: 25 had both consultations and electrocardiograms, and 24 had electrocardiograms only. The rate of cardiac anomalies among the cocaine-positive infants was significantly higher (relative risk = 3.7; 95% confidence interval: (1.4, 9.4)) than the rate of these anomalies among the cocaine-negative comparison group (65/100 vs 18/1000); the rate for cocaine-positive infants was also significantly higher than published rates for general populations of infants. Several electrocardiographic abnormalities, high-grade ventricular ectopy, and cardiorespiratory arrests were also noted in our study population. We conclude that cocaine exposure during prenatal life appears to predispose infants to structural cardiovascular malformations, electrocardiographic abnormalities, and, possibly, cardiopulmonary autonomic dysfunction.

Safety and Efficacy of Low-Potassium Dialysate

To evaluate the safety and efficacy of low-potassium dialysate, 11 patients with stable end-stage renal disease and with no history of arrhythmia or digitalis use were studied. All were treated with hemodialysis three times per week. Dialysates with potassium concentrations of 2 mEq/L, 1 mEq/L, or 0 mEq/L were compared. Each patient (exceptions noted in text) was studied once at each bath potassium concentration. Cardiac rhythm was recorded by Holter monitor during and for six hours following dialysis. Single PVCs and APCs were common with all potassium concentrations. Only one patient had high-grade ventricular ectopy. It was seen with each of the three potassium concentrations, but was most severe with the potassium-free dialysate. The potassium-free dialysate removed significantly more potassium (78.5 +/- 2.6 mEq) than the 1-K dialysate (62.9 +/- 5.1 mEq) or the 2-K dialysate (50.6 +/- 6 mEq), and the 1-K dialysate removed significantly more potassium than the 2-K dialysate. There were small but significant differences in serum potassium concentrations with the three different dialysates. It was concluded that (1) in all but one of our patients potassium-free dialysate did not produce new ectopy; (2) potassium-free dialysate was 24% more effective than 1-K dialysate and 50% more effective than 2-K dialysate in removing body potassium; and (3) 1-K dialysate was 20% more effective than 2-K dialysate in removing body potassium.

Cardiomyopathy of Duchenne muscular dystrophy.

A total of 18 male patients with Duchenne muscular dystrophy (DMD), aged 8-29 years (mean, 15.7 years), were prospectively studied to assess the cardiomyopathy associated with DMD, using clinical parameters and noninvasive cardiovascular investigations: electrocardiogram (ECG), Holter monitoring, and echocardiography. In addition, five clinical tests of cardiovascular autonomic function were used to assess the role of the autonomic nervous system in the pathogenesis of dysrhythmias. The majority of subjects were asymptomatic, but four had abnormal physical findings. All had abnormal ECG, the commonest abnormality (in 16) being tall R waves or increased R/S ratios in the right precordial leads; 14 had abnormal findings on echocardiography, including three with poor left ventricular function and five with mitral valve prolapse (MVP). Labile abrupt sinus tachycardia was present in 11, and four had high-grade ventricular ectopy. None had definite clinical evidence of autonomic dysfunction. The cardiomyopathy of DMD appears to be unrelated to disease severity. However, abnormal Q waves or Q/R ratios in ECG leads I, aVL9 and V5-V6 are significantly related to young age (p less than 0.05), and high-grade ventricular ectopy occurred significantly more frequently (p less than 0.05) in older subjects (greater than 15 years). Dysrhythmias were not related to the presence of MVP, poor left ventricular function, or autonomic dysfunction.

Long‐Term Outcome Following Programmed Electrical Stimulation in Patients with High‐Grade Ventricular Ectopy

To determine if programmed electrical stimulation (PES) could be utilized to identify patients with high-grade ventricular ectopy at low- or high-risk for sudden cardiac death, we performed PES in 40 patients with high-grade ventricular ectopy refractory to conventional antiarrhythmic agents. Twenty-one patients had a previous myocardial infarction, five had cardiomyopathy, six had hypertension, three had valvular heart disease and five had no known structural heart disease. The mean age was 50 years (range, 18 to 76). During programmed ventricular stimulation, eight patients had inducible sustained (more than 30 seconds) monomorphic ventricular tachycardia (Group I) but in 32 patients sustained ventricular tachycardia was not inducible (Group II). None of the five patients without structural heart disease were inducible while seven out of 21 (33%) patients with previous myocardial infarction had inducible ventricular tachycardia (VT). Antiarrhythmic therapy was instituted in patients with inducible VT; patients without inducible VT did not receive antiarrhythmic agents. In Group I, seven of the eight patients are alive (mean follow-up, 16 months) and in Group II, 28 of the 32 patients are alive (mean follow-up, 17 months). None of the five deaths were sudden. We conclude that in the absence of antiarrhythmic therapy, the incidence of sudden cardiac death is very low in patients with high-grade ventricular ectopy who do not have inducible monomorphic ventricular tachycardia during programmed ventricular stimulation.

Antiarrhythmic effects of oral indecainide in patients with ventricular tachyarrhythmias.

In order to assess the efficacy and safety of oral indecainide in patients with serious ventricular arrhythmias we studied 11 patients with high-grade ventricular ectopy and ventricular tachycardia (VT) which were refractory to therapy with at least one standard antiarrhythmic drug. Spontaneous arrhythmias were quantitated by 24-h Holter monitor before and during therapy with indecainide. Spontaneous VT was sustained in 4 patients and nonsustained in 7. Ten patients underwent baseline electrophysiologic study (EPS) and VT was induced in 9. The mean ejection fraction was 25 +/- 14%. Indecainide was given orally at a dose of 211 +/- 118 mg/day. The frequency of ventricular premature beats (VPBs) was significantly (greater than 85%) decreased in 90% of patients, while ventricular couplets frequency decreased in 78%. Spontaneous VT was abolished in 5 of 11 (45%). Sustained VT was induced in 5 of 7 (71%) patients who underwent follow-up EPS. The QRS duration was significantly prolonged during therapy (0.13 +/- 0.04 s) compared to control (0.10 +/- 0.02 s). The PR, QTc, and JTc intervals were not significantly changed. Indecainide was well tolerated, but 2 patients died of ventricular tachyarrhythmias while receiving the drug. Indecainide suppressed VPBs in a high percentage of patients, but was much less successful in controlling VT. Caution is necessary when using this drug because of its potential for exacerbation of arrhythmia.

Ventricular Arrhythmia: Management Strategy

The management of ventricular arrhythmia continues to be one of the most difficult therapeutic problems in medicine today. Both invasive and noninvasive techniques have demonstrated success in management of patients at high risk for sudden cardiac death. High-risk subgroups include patients who have experienced sudden cardiac death and have been resuscitated successfully, patients with high-grade ventricular ectopy associated with left ventricular dysfunction, and patients who have had recent myocardial infarction. Traditional and experimental antiarrhythmic agents are available to the clinician, and in some patients combination therapy may prove more useful than application of a single agent alone. In individuals in whom pharmacologic intervention fails, map-guided surgical excision may be beneficial. The application of the automatic implantable defibrillator appears to have promise in truly refractory situations.

111 HEMODYNAMIC ASSESSMENT OF PULMONARY INSUFFICIENCY AFTER TETRALOGY OF FALLOT REPAIR

Pulmonary insufficiency (PI) has been implicated in the etiology of VPCs and biventricular dysfunction after repair of Tetralogy of Fallot (TF). To assess this, 50 consecutive postop TF patients with clinical PI were evaluated prospectively with branch pulmonary artery (PA) angiography at follow-up catheterization. Group I consisted of 23 pts who cleared contrast from the right heart normally, within 2 beats of injection; Group II consisted of 27 pts who required 3-12 beats to clear the right heart (x=6). Groups did not differ significantly in age at surgery or evaluation, or in residual RV hypertension. They were compared for RV size by M-mode echocardiography using RV/LV diastolic dimension ratio, for RV and LV ejection fractions (EF) by radionuclide ventriculography, and for grade of VPCs on treadmill exercise and/or ambulatory EGG. Findings are summarized below: In this study, prolonged right heart opacification after branch PA injection correlated significantly with RV dilatation, biventricular dysfunction and high grade ventricular ectopy. After TF repair, branch PA angiography provides a useful adjunctive method of assessing the variable impact of pulmonary insufficiency.

Ventricular arrhythmias and mitral valve prolapse in childhood

Although ventricular arrhythmias are well described in adults with mitral valve prolapse, this association remains controversial in children. To assess the incidence of ventricular premature complexes (VPCs), 103 consecutive children with mitral valve (MV) prolapse confirmed by echocardiography were evaluated prospectively by treadmill exercise and ambulatory ECG. A group of 50 normal children with clinical, ECG, or echocardiographic evidence of heart disease who had undergone treadmill exercise and ambulatory ECG served as controls. In the group with MV prolapse, 16 patients had VPCs with treadmill exercise and 39 had VPCs on ambulatory ECG. High-grade ventricular ectopy (multiform VPCs, couplets, or ventricular tachycardia) was recorded in four patients with MV prolapse during treadmill exercise and in eight during ambulatory ECG. In contrast, no control patient had a single VPC in response to treadmill exercise and only four control patients had rare uniform VPCs on ambulatory ECG. Neither physical examination findings, standard ECG results, nor symptoms could be correlated with VPCs in the patients with MV prolapse. Although the prognostic implications of these findings are uncertain, this study demonstrates that potentially serious ventricular arrhythmias are frequently observed in children with MV prolapse.

Clinical correlations in patients with acute myocardial infarction and left ventricular thrombus detected by two-dimensional echocardiography

Eleven of forty-nine patients with acute myocardial infarction had left ventricular thrombus identified by two-dimensional echocardiography. The patients with thrombi had a greater incidence of transmural infarction, high-grade ventricular ectopy on ambulatory monitoring and lower radionuclide ejection fractions than the patients without thrombi. Most of the patients were receiving full-dose heparin and/or warfarin anticoagulation from the time of admission to the hospital. Thus the thrombi either developed prior to hospital admission or developed during anticoagulation therapy. Two patients with thrombi had peripheral emboli complicating their infarction. One of these patients was undergoing anticoagulation at the time of his embolus.