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Barry J Maron

Publications and source records attributed to Barry J Maron.

At least 91 records · Page 5Linked to original sources
PubMed2003

Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy.

BACKGROUND: The influence of left ventricular outflow tract obstruction on the clinical outcome of hypertrophic cardiomyopathy remains unresolved. METHODS: We assessed the effect of outflow tract obstruction on morbidity and mortality in a large cohort of patients with hypertrophic cardiomyopathy who were followed for a mean (+/-SD) of 6.3+/-6.2 years. RESULTS: Of the 1101 consecutive patients, 273 (25 percent) had obstruction of left ventricular outflow under basal (resting) conditions with a peak instantaneous gradient of at least 30 mm Hg. A total of 127 patients (12 percent) died of hypertrophic cardiomyopathy, and 216 surviving patients (20 percent) had severe, disabling symptoms of progressive heart failure (New York Heart Association [NYHA] functional class III or IV). The overall probability of death related to hypertrophic cardiomyopathy was significantly greater among patients with outflow tract obstruction than among those without obstruction (relative risk, 2.0; P=0.001). The risk of progression to NYHA class III or IV or death specifically from heart failure or stroke was also greater among patients with obstruction (relative risk, 4.4; P<0.001), particularly among patients 40 years of age or older (P<0.001). Age-adjusted multivariate analysis confirmed that outflow tract obstruction was independently associated with an increased risk of both death related to hypertrophic cardiomyopathy (relative risk, 1.6; P=0.02) and progression to NYHA class III or IV or death from heart failure or stroke (relative risk, 2.7; P<0.001). The likelihood of severe symptoms and death related to outflow tract obstruction did not increase as the gradient increased above the threshold of 30 mm Hg. CONCLUSIONS: In patients with hypertrophic cardiomyopathy, left ventricular outflow tract obstruction at rest is a strong, independent predictor of progression to severe symptoms of heart failure and of death.

Adult↗
PubMed2003

Upper and lower limits of vulnerability to sudden arrhythmic death with chest-wall impact (commotio cordis).

OBJECTIVES: In an animal model of commotio cordis, sudden death with chest-wall impact, we sought to systematically evaluate the importance of impact velocity in the generation of ventricular fibrillation (VF) with baseball chest-wall impact. BACKGROUND: Sudden cardiac death can occur with chest-wall blows in recreational and competitive sports (commotio cordis). Analyses of clinical events suggest that the energy of impact is often not of unusual force, although this has been difficult to quantify. METHODS: Juvenile swine (8 to 25 kg) were anesthetized, placed prone in a sling to receive chest-wall strikes during the vulnerable time window during repolarization for initiation of VF with a baseball propelled at 20 to 70 mph. RESULTS: Impacts at 20 mph did not induce VF; incidence of VF increased incrementally from 7% with 25 mph impacts, to 68% with chest impact at 40 mph, and then diminished at >/=50 mph (p < 0.0001). Peak left ventricular pressure generated by the chest blow was related to the incidence of VF in a similar Gaussian relationship (p < 0.0001). CONCLUSIONS: The energy of impact is an important variable in the generation of VF with chest-wall impacts. Impacts at 40 mph were more likely to produce VF than impacts with greater or lesser velocities, suggesting that the predilection for commotio cordis is related in a complex manner to the precise velocity of chest-wall impact.

Animals↗
PubMed2003

Automated external defibrillator arrhythmia detection in a model of cardiac arrest due to commotio cordis.

INTRODUCTION: Cardiac arrest due to chest wall blows (commotio cordis) has been reported with increasing frequency in children, and only about 15% of victims survive. Automated external defibrillators (AEDs) have been shown to be life saving in adults with cardiac arrest, but data on their use in children are limited. In a swine model of commotio cordis designed to be most relevant to young children, we assessed the efficacy of a commercially available AED for recognition and termination of ventricular fibrillation. METHODS AND RESULTS: Ventricular fibrillation was produced in anesthetized juvenile swine by precordial impact from a baseball under controlled conditions. Animals were randomized to defibrillation after 1, 2, 4, or 6 minutes of ventricular fibrillation. Twenty-six swine underwent 50 ventricular fibrillation inductions. Sensitivity of the AED for recognition of ventricular fibrillation was 98%, and specificity for nonshockable episodes was 100%. All episodes of ventricular fibrillation were successfully terminated by the AED. CONCLUSION: In this experimental model of commotio cordis, the AED proved to be highly sensitive and specific for recognition of ventricular fibrillation and effective in terminating the arrhythmia and restoring sinus rhythm. These findings suggest that early defibrillation with the AED could save young lives on the athletic field.

Animals↗
PubMed2003

Drug-induced toxic myocarditis.

A 66-year-old woman presented with new-onset complete left bundle branch block and congestive heart failure. She had had chronic paranoid schizophrenia for 35 years and had been taking medications to control her psychiatric disorder for the past 10 years. A 2-dimensional echocardiogram performed at the onset of congestive heart failure showed dilated cardiomyopathy with global impairment of left ventricular function (ejection fraction <0.25). Despite withdrawal of the medications most likely responsible for the heart problems (perphenazine, 2 mg; and amitriptyline, 25 mg), the patient died of refractory congestive heart failure 2 years later. Histologic examination at autopsy showed evidence of persistent toxic myocarditis with fibrosis of the heart and persistent chronic hepatitis. These autopsy findings were considered to be drug related.

Adrenergic Uptake Inhibitors↗
PubMed2002

Physiologic limits of left ventricular hypertrophy in elite junior athletes: relevance to differential diagnosis of athlete's heart and hypertrophic cardiomyopathy.

OBJECTIVES: The present study was undertaken to define physiologic limits of left ventricular hypertrophy in elite adolescent athletes. BACKGROUND: Systematic sports training may cause increased left ventricular wall thickness (LVWT), creating uncertainty regarding the differential diagnosis of athlete's heart from hypertrophic cardiomyopathy (HCM). This distinction is crucial because HCM is responsible for about one-third of all sudden deaths in young athletes. Echocardiographic data defining athlete's heart are limited largely to adults, with little information specifically in adolescent athletes (14 to 18 years old), for whom the risk of sudden death from HCM is highest. METHODS: Seven hundred and twenty elite adolescent athletes (75% male) aged 15.7 +/- 1.4 years participating in ball, racket, and endurance sports and 250 healthy sedentary controls of similar age, gender, and body surface area underwent echocardiography. RESULTS: Compared with controls, athletes had greater absolute LVWT (9.5 +/- 1.7 mm vs. 8.4 +/- 1.4 mm; p < 0.0001). Maximal LVWT exceeded predicted upper limits in 38 athletes (5%); however, no female athlete had a LVWT >11 mm and only three trained male athletes had absolute LVWT >12 mm (0.4%). Each of the 38 athletes with a LVWT exceeding predicted limits also showed enlarged left ventricular cavity dimension (54.4 +/- 2.1 mm; range 52 to 60 mm). CONCLUSIONS: Trained adolescent athletes demonstrated greater absolute LVWT compared with nonathletes. Only a small proportion of athletes exhibited a LVWT exceeding upper limits, very rarely >12 mm, and then always with chamber enlargement. Hypertrophic cardiomyopathy should be considered strongly in any trained adolescent male athlete with LVWT >12 mm (females >11 mm) and nondilated left ventricle.

Adolescent↗
PubMed2002

Long-term clinical significance of frequent and complex ventricular tachyarrhythmias in trained athletes.

OBJECTIVES: The aim of this study was to clarify the clinical relevance of ventricular tachyarrhythmias assessed by 24-h ambulatory electrocardiograms (ECG) in a large, unique, and prospectively evaluated athletic population. BACKGROUND: For athletes with ventricular tachyarrhythmias, the risk of sudden cardiac death associated with participation in competitive sports is unresolved. METHODS; We assessed 355 competitive athletes with ventricular arrhythmias (VAs) on a 24-h ambulatory (Holter) ECG that was obtained because of either palpitations, the presence of > or = 3 premature ventricular depolarizations (PVDs) on resting 12-lead ECG, or both. RESULTS: Athletes were segregated into three groups: Group A with > or = 2,000 PVDs/24 h (n = 71); Group B with > or = 100 <2,000 PVDs/24 h (n = 153); and Group C with only <100 PVDs/24 h (n = 131). Cardiac abnormalities were detected in 26 of the 355 study subjects (7%) and were significantly more common in Group A (21/71, 30%) than in Group B (5/153, 3%) or Group C athletes (0/131, 0% p < 0.001). Only the 71 athletes in Group A were excluded from competition. During follow-up (mean, 8 years), 70 of 71 athletes in Group A and each of the 284 athletes in Groups B and C have survived without cardiovascular events. The remaining Group A athlete died suddenly of arrhythmogenic right ventricular cardiomyopathy while participating in a field hockey game against medical advice. Frequent and complex ventricular tachyarrhythmias are common in trained athletes and are usually unassociated with underlying cardiovascular abnormalities. Such VAs (when unassociated with cardiovascular abnormalities) do not convey adverse clinical significance, appear to be an expression of "athlete's heart syndrome," and probably do not per se justify a disqualification from competitive sports.

Adolescent↗
PubMed2002

Assessment of diastolic function with Doppler tissue imaging to predict genotype in preclinical hypertrophic cardiomyopathy.

BACKGROUND: Unexplained left ventricular hypertrophy (LVH) is considered diagnostic of hypertrophic cardiomyopathy (HCM) but fails to identify all genetically affected individuals. Altered diastolic function has been hypothesized to represent an earlier manifestation of HCM before the development of LVH; however, data regarding the clinical utility of imaging techniques that assess this parameter are limited. METHODS AND RESULTS: Echocardiographic studies including Doppler tissue imaging (DTI) were performed in a genotyped HCM population with beta-myosin heavy chain (beta -MHC) mutations. Genotype (+) individuals with LVH (G+/LVH+; n=18) and genotype (+) individuals without LVH (G+/LVH-; n=18) were compared with normal control subjects (n=36). Left ventricular ejection fraction (EF) was significantly higher in both genotype (+) groups (75+/-5% and 71+/-6%, respectively, versus 64+/- 5% in control subjects; P<0.0001). Mean early diastolic myocardial velocities (Ea) were significantly lower in both genotype (+) subgroups, irrespective of LVH (P<0.02). However, there was substantial overlap in Ea velocities between the G+/LVH- and control groups. An Ea velocity of < or =13.5 cm/s had 86% specificity and 75% sensitivity for identifying genotype-positive subjects. The combination of EF > or =68% and Ea velocity <15 cm/s was 100% specific and 44% sensitive in predicting affected genotype. CONCLUSIONS: Abnormalities of diastolic function assessed by Doppler tissue imaging precede the development of LVH in individuals with HCM caused by beta -MHC mutations. Although Ea velocity alone was not sufficiently sensitive as a sole diagnostic criterion, the combination of Ea velocity and EF was highly predictive of affected genotype in individuals without overt manifestations of HCM.

Adult↗
PubMed2002

Hypertrophic cardiomyopathy: a systematic review.

CONTEXT: Throughout the past 40 years, a vast and sometimes contradictory literature has accumulated regarding hypertrophic cardiomyopathy (HCM), a genetic cardiac disease caused by a variety of mutations in genes encoding sarcomeric proteins and characterized by a broad and expanding clinical spectrum. OBJECTIVES: To clarify and summarize the relevant clinical issues and to profile rapidly evolving concepts regarding HCM. DATA SOURCES: Systematic analysis of the relevant HCM literature, accessed through MEDLINE (1966-2000), bibliographies, and interactions with investigators. STUDY SELECTION AND DATA EXTRACTION: Diverse information was assimilated into a rigorous and objective contemporary description of HCM, affording greatest weight to prospective, controlled, and evidence-based studies. DATA SYNTHESIS: Hypertrophic cardiomyopathy is a relatively common genetic cardiac disease (1:500 in the general population) that is heterogeneous with respect to disease-causing mutations, presentation, prognosis, and treatment strategies. Visibility attached to HCM relates largely to its recognition as the most common cause of sudden death in the young (including competitive athletes). Clinical diagnosis is by 2-dimensional echocardiographic identification of otherwise unexplained left ventricular wall thickening in the presence of a nondilated cavity. Overall, HCM confers an annual mortality rate of about 1% and in most patients is compatible with little or no disability and normal life expectancy. Subsets with higher mortality or morbidity are linked to the complications of sudden death, progressive heart failure, and atrial fibrillation with embolic stroke. Treatment strategies depend on appropriate patient selection, including drug treatment for exertional dyspnea (beta-blockers, verapamil, disopyramide) and the septal myotomy-myectomy operation, which is the standard of care for severe refractory symptoms associated with marked outflow obstruction; alcohol septal ablation and pacing are alternatives to surgery for selected patients. High-risk patients may be treated effectively for sudden death prevention with the implantable cardioverter-defibrillator. CONCLUSIONS: Substantial understanding has evolved regarding the epidemiology and clinical course of HCM, as well as novel treatment strategies that may alter its natural history. An appreciation that HCM, although an important cause of death and disability at all ages, does not invariably convey ominous prognosis and is compatible with normal longevity should dictate a large measure of reassurance for many patients.

Cardiomyopathy, Hypertrophic↗
PubMed2002

Clinical profile and spectrum of commotio cordis.

CONTEXT: Although blunt, nonpenetrating chest blows causing sudden cardiac death (commotio cordis) are often associated with competitive sports, dangers implicit in such blows can extend into many other life activities. OBJECTIVE: To describe the comprehensive spectrum of commotio cordis events. DESIGN AND SETTING: Analysis of confirmed cases from the general community assembled in the US Commotio Cordis Registry occurring up to September 1, 2001. MAIN OUTCOME MEASURE: Commotio cordis event. RESULTS: Of 128 confirmed cases, 122 (95%) were in males and the mean (SD) age was 13.6 (8.2) years (median, 14 years; range, 3 months to 45 years); only 28 (22%) cases were aged 18 years or older. Commotio cordis events occurred most commonly during organized sporting events (79 [62%]), such as baseball, but 49 (38%) occurred as part of daily routine and recreational activities. Fatal blows were inflicted with a wide range of velocities but often occurred inadvertently and under circumstances not usually associated with risk for sudden death in informal settings near the home or playground. Twenty-two (28%) participants were wearing commercially available chest barriers, including 7 in whom the projectile made direct contact with protective padding (baseball catchers and lacrosse/hockey goalies), and 2 in whom the projectile was a baseball specifically designed to reduce risk. Only 21 (16%) individuals survived their event, with particularly prompt cardiopulmonary resuscitation/defibrillation (most commonly reversing ventricular fibrillation) the only identifiable factor associated with a favorable outcome. CONCLUSIONS: The expanded spectrum of commotio cordis illustrates the potential dangers implicit in striking the chest, regardless of the intent or force of the blow. These findings also suggest that the safety of young athletes will be enhanced by developing more effective preventive strategies (such as chest wall barriers) to achieve protection from ventricular fibrillation following precordial blows.

Adolescent↗
PubMed2002

Remodeling of left ventricular hypertrophy in elite athletes after long-term deconditioning.

BACKGROUND: The clinical significance and long-term consequences of left ventricular (LV) hypertrophy associated with intensive athletic conditioning remain unresolved. METHODS AND RESULTS: We prospectively evaluated 40 elite male athletes who had shown marked LV cavity enlargement of > or = 60 mm, wall thickness of > or = 13 mm, or both in a longitudinal fashion with serial echocardiograms, initially at peak training (age 24 +/- 4 years) and subsequently after a long-term deconditioning period (1 to 13 years; mean, 5.6 +/- 3.8). After detraining, LV cavity dimension decreased by 7% (61.2 +/- 2.9 to 57.2 +/- 3.1 mm; P<0.001), maximum wall thickness by 15% (12.0 +/- 1.3 to 10.1 +/- 0.8 mm; P<0.001), and mass normalized to height by 28% (194 +/- 25 to 140 +/- 21 g/m; P<0.001). However, individual subject analysis showed persistent substantial cavity dilatation (> or = 60 mm) in 9 athletes (22%); in contrast, wall thickness returned to normal in each athlete. Multiple regression analysis demonstrated that approximately 50% of the incomplete reduction in cavity dimension was explained by increased body weight and recreational physical activity performed during the follow-up period. No athlete had developed cardiac symptoms, impaired exercise performance, or evidence of LV dysfunction. CONCLUSIONS: LV remodeling was evident after long-term detraining, with significant reduction in cavity size and normalization of wall thickness. Resolution of cavity enlargement was, however, incomplete in most cases, and substantial chamber dilatation persisted in >20% of athletes. The possibility that this residual LV hypertrophy, apparently part of the athlete's heart syndrome, may have future long-term clinical implications in some individuals cannot be excluded with certainty.

Adaptation, Physiological↗