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Biomedical subjects

B J Maron

Publications and source records attributed to B J Maron.

At least 91 records · Page 5Linked to original sources
PubMed1997

Lutembacher's syndrome.

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Echocardiography, Doppler, Color↗
PubMed1996

Athlete's heart in women. Echocardiographic characterization of highly trained elite female athletes.

UNLABELLED: OBJECTIVES; To define the expression of "athlete's heart" in women by determining the alterations in cardiac dimensions associated with long-term intense conditioning in elite female athletes. DESIGN; Prospective cardiovascular assessment conducted from 1986 through 1993. Subjects were evaluated using 2-dimensional, M-mode, and Doppler echo-cardiographic studies. SETTING: Institute of Sports Science, Italian National Olympic Committee, Rome, Italy. PARTICIPANTS: A total of 600 elite female athletes (mean age, 21 years; range, 12-49 years) who had participated in vigorous training (mean duration, 9 years; range, 2-32 years) and had competed in 27 sports, including 211 athletes at the international level and 389 at the national level. A control group consisted of 65 sedentary volunteer women (mean age, 23.7 years; range, 14-41 years) who were free of cardiovascular disease and who did not participate in regular athletic training. MAIN OUTCOME MEASURES: Left ventricular end-diastolic cavity dimension and wall thickness. RESULTS: Athletes demonstrated larger left ventricular end-diastolic cavity dimension (mean +/- SD) (49 +/- 4 mm) and greater maximal wall thickness (8.2 +/- 0.9 mm) than controls (46 +/- 3 mm and 7.2 +/- 0.6 mm; P < .001). These dimensions were 6% and 14% larger in athletes. Among athletes, left ventricular cavity dimension was 40 mm to 66 mm, exceeded normal limits ( > 54 mm) in 47 women (8%), and was within the range consistent with primary dilated cardiomyopathy ( > or = 60 mm) in 4 athletes (1%). Training for endurance sports, such as cycling, cross-country skiing, and rowing had the greatest effect on cavity dimension. Left ventricular wall thickness was 6 mm to 12 mm in athletes and did not exceed normal limits or extend into the borderline gray zone with hypertrophic cardiomyopathy in any subject. Compared with data from 738 previously studied male athletes, female athletes showed significantly smaller left ventricular cavity dimension (11% less; P < .001) and wall thickness (23% less; P < .001). CONCLUSIONS: Highly trained women athletes frequently demonstrate cardiac dimensional changes as an adaptation to physical training, although absolute left ventricular cavity size exceeding normal limits was evident in a minority (8%) of women athletes and was rarely (1% of athletes) within the range of dilated cardiomyopathy. Athletic training was not a stimulus for substantial increases in absolute left ventricular wall thickness, which was within normal limits for all women athletes. These findings suggest that the clinical differentiation of athlete's heart and hypertrophic cardiomyopathy appears to be a diagnostic dilemma that is limited to male athletes.

Adolescent↗
PubMed1996

Sudden death in young competitive athletes. Clinical, demographic, and pathological profiles.

OBJECTIVE: To develop clinical, demographic, and pathological profiles of young competitive athletes who died suddenly. DESIGN: Systematic evaluation of clinical information and circumstances associated with sudden deaths; interviews with family members, witnesses, and coaches; and analyses of postmortem anatomic, microscopic, and toxicologic data. PARTICIPANTS AND SETTING: A total of 158 sudden deaths that occurred in trained athletes throughout the United States from 1985 through 1995 were analyzed. MAIN OUTCOME MEASURES--Characteristics and probable cause of death. RESULTS: Of 158 sudden deaths among athletes, 24 (15%) were explained by noncardiovascular causes. Among the 134 athletes who had cardiovascular causes of sudden death, the median age was 17 years (range, 12-40 years), 120 (90%) were male, 70 (52%) were white, and 59 (44%) were black. The most common competitive sports involved were basketball (47 cases) and football (45 cases), together accounting for 68% of sudden deaths. A total of 121 athletes (90%) collapsed during or immediately after a training session (78 cases) or a formal athletic contest (43 cases), with 80 deaths (63%) occurring between 3 PM and 9 PM. The most common structural cardiovascular diseases identified at autopsy as the primary cause of death were hypertrophic cardiomyopathy (48 athletes [36%]), which was disproportionately prevalent in black athletes compared with white athletes (48% vs 26% of deaths; P = .01), and malformations involving anomalous coronary artery origin (17 athletes [13%]). Of 115 athletes who had a standard preparticipation medical evaluation, only 4 (3%) were suspected of having cardiovascular disease, and the cardiovascular abnormality responsible for sudden death was correctly identified in only 1 athlete (0.9%). CONCLUSIONS: Sudden death in young competitive athletes usually is precipitated by physical activity and may be due to a heterogeneous spectrum of cardiovascular disease, most commonly hypertrophic cardiomyopathy. Preparticipation screening appeared to be of limited value in identification of underlying cardiovascular abnormalities.

Adolescent↗
PubMed1996

Risk for sudden cardiac death associated with marathon running.

OBJECTIVES: This analysis was performed to quantitatively assess the relative risks, associated with underlying cardiovascular disease, incurred in the course of intense competitive sports. BACKGROUND: Sudden cardiac death during athletic activities is a highly visible event, and controversy persists regarding the true risks associated with participation in sports. METHODS: The prevalence of sudden death was assessed in two systematically tabulated groups of endurance runners competing in the annual Marine Corps (1976 to 1994) and Twin Cities (1982 to 1994) marathons, held over a cumulative 30-year period. RESULTS: A total of 215,413 runners completed the races, and four exercise-related sudden deaths occurred, each due to unsuspected structural cardiovascular disease. Three deaths occurred during the race (after 15 to 24 miles [24 to 38.4 km]) and the other immediately after its completion. The ages were 19 to 58 years (average 37), and three were men. Three of the sudden deaths were due to atherosclerotic coronary artery disease (narrowing of two or three vessels) and one to anomalous origin of the left main coronary artery from the right sinus of Valsalva. None of the four runners had prior documentation of heart disease or experienced prodromal symptoms, and two had previously completed three marathon races each. The overall prevalence of sudden cardiac death during the marathon was only 0.002%, strikingly lower than for several other variables of risk for premature death calculated for the general U.S. population. CONCLUSIONS: Although highly trained athletes such as marathon runners may harbor underlying and potentially lethal cardiovascular disease, the risk for sudden cardiac death associated with such intense physical effort was exceedingly small (1 in 50,000) and as little as 1/100th of the annual overall risk associated with living, either with or without heart disease. The low risk for sudden death identified in long-distance runners from the general population suggests that routine screening for cardiovascular disease in such athletic populations may not be justifiable.

Adult↗
PubMed1996

Triggers for sudden cardiac death in the athlete.

Sudden death on the athletic field is usually due to underlying cardiovascular disease. Coronary artery disease is most common in older athletes, and a variety of congenital cardiovascular malformations predominate in young competitive athletes. Of these lesions, the most common in North America is hypertrophic cardiomyopathy. A variety of coronary artery anomalies are next in frequency, with the most important being anomalous origin of left main coronary artery from the anterior sinus of Valsalva.

Cardiomyopathy, Hypertrophic↗
PubMed1995

Hypertrophic cardiomyopathy in Tuscany: clinical course and outcome in an unselected regional population.

OBJECTIVES: Our aim was to study a population of patients with hypertrophic cardiomyopathy from the well defined geographic region of Tuscany in central Italy, a group virtually free of selective referral bias and therefore probably closely representative of the true patient population with this disease. BACKGROUND: Most available information on clinical course, natural history and prognosis of hypertrophic cardiomyopathy is based on data generated from tertiary referral centers and therefore constitutes a potentially biased perspective of the disease process in this complex and diverse condition. METHODS: The study group comprised 202 patients aged 1 to 74 years (mean +/- SD 41 +/- 17) at initial diagnosis and followed up for 1 to 30 years (mean 10 +/- 5). RESULTS: Largely with the use of single or multiple drug therapy, the vast majority of patients (n = 154 [76%]) were asymptomatic or mildly symptomatic and in stable or improved condition over the period of follow-up, whereas the remaining patients (n = 48 [24%]) experienced deterioration, had substantial functional impairment or died. Of the 13 patients (6%) who died of cardiovascular causes related to hypertrophic cardiomyopathy, 11 had progressive congestive heart failure (including 6 in the end-stage phase) and only 2 died suddenly. The annual mortality rate for cardiovascular disease was 0.6% and that due to sudden cardiac death was only 0.1%; the cumulative survival rate was 97%, 95% and 92%, respectively, at 5, 10 and 15 years of follow-up. Atrial fibrillation proved to be a relatively common (n = 57 [28%]) and particularly unfavorable clinical feature, with premature death occurring in 9 of the 57 patients. The cumulative survival rate after 15 years was 76% for patients with atrial fibrillation versus 97% for patients with sinus rhythm. Syncope occurred in 33 patients (16%) but did not appear to be of prognostic significance. CONCLUSIONS: In an unselected regional population, hypertrophic cardiomyopathy had a relatively benign prognosis inconsistent with its prior characterization as a generally progressive disorder, based primarily on the experience of selected referral institutions. Sudden unexpected cardiac death was distinctly uncommon, although a sizable proportion of patients (particularly the subset prone to atrial fibrillation), did experience clinical deterioration.

Adolescent↗
PubMed1995

Echocardiographic assessment of spontaneously occurring feline hypertrophic cardiomyopathy. An animal model of human disease.

BACKGROUND: Necropsy studies in domestic cats have suggested the occurrence of a primary cardiac disease resembling hypertrophic cardiomyopathy (HCM) in humans. We used two-dimensional echocardiography to define morphological and functional features of HCM during life in 46 domestic cats evaluated in a subspecialty veterinary clinic. Cats were 8 months to 14 years old (mean, 6 years). METHODS AND RESULTS: During the follow-up period of as long as 49 months, 18 cats died (or were euthanatized) due to congestive heart failure, peripheral embolization, or both, and 3 other cats experienced out-of-hospital sudden, unexpected death. Echocardiography showed a small left ventricular cavity, associated with a variety of patterns of hypertrophy. Wall thickening was most often diffuse (involving ventricular septum and free wall) in 31 cats (67%) and segmental in 15 (33%), including 12 with thickening confined to anterior septum; wall thickening was judged to be asymmetrical in 42 and symmetrical (concentric) in 4. In 30 cats (65%), marked mitral valve systolic anterior motion produced dynamic obstruction to left ventricular outflow (Doppler estimated gradients, 25 to 110 mm Hg). Compared with survivors, cats with HCM that died with heart failure had greater left ventricular thickness (8.1 +/- 1.5 versus 7.3 +/- 0.9 mm; P < .05) and larger left atria (20.1 +/- 4.6 versus 16.8 +/- 3.4 mm; P = .01) and more often had the nonobstructive form (89% versus 48%; P < .01). CONCLUSIONS: A spontaneously occurring disease of domestic cats was identified by echocardiography and was similar in its phenotypic expression to HCM in humans; it was characterized by unexplained left ventricular hypertrophy in a variety of patterns with or without evidence of outflow obstruction. Unfavorable prognosis was associated with greater magnitude of hypertrophy and absence of outflow obstruction. Feline HCM may prove to be a valuable animal model of the human disease.

Animals↗
PubMed1995

Prevalence of hypertrophic cardiomyopathy in a general population of young adults. Echocardiographic analysis of 4111 subjects in the CARDIA Study. Coronary Artery Risk Development in (Young) Adults.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is a genetically transmitted disease and an important cause of morbidity and sudden cardiac death in young people, including competitive athletes. At present, however, few data exist to estimate the prevalence of this disease in large populations. METHODS AND RESULTS: As part of the Coronary Artery Risk Development in (Young) Adults (CARDIA) Study, an epidemiological study of coronary risk factors, 4111 men and women 23 to 35 years of age selected from the general population of four urban centers had technically satisfactory echocardiographic studies during 1987 through 1988. Probable or definite echocardiographic evidence of HCM was present in 7 subjects (0.17%) on the basis of identification of a hypertrophied, nondilated left ventricle and maximal wall thickness > or = 15 mm that were not associated with systemic hypertension. Prevalence in men and women was 0.26:0.09%; in blacks and whites, 0.24:0.10%. Ventricular septal thickness was 15 to 21 mm (mean, 17 mm) in the 7 subjects. Only 1 of the 7 subjects had ever experienced important cardiac symptoms attributable to HCM, had previously been suspected of having cardiovascular disease, or had obstruction to left ventricular outflow; 4 other subjects had relatively mild systolic anterior motion of the mitral valve that was insufficient to produce dynamic basal outflow obstruction. ECGs were abnormal in 5 of the 7 subjects. Five other study subjects had left ventricular wall thicknesses of 15 to 21 mm that were a consequence of systemic hypertension. CONCLUSIONS: HCM was present in about 2 of 1000 young adults. These unique population-based data will aid in assessments of the impact of HCM-related mortality and morbidity in the general population and the practicality of screening large populations for HCM, including those comprising competitive athletes.

Adolescent↗
PubMed1995

Blunt impact to the chest leading to sudden death from cardiac arrest during sports activities.

BACKGROUND: Sudden death from cardiac arrest in a young person may occur during sports play after a blunt blow to the chest in the absence of structural cardiovascular disease or traumatic injury (cardiac concussion or commotio cordis). We studied the clinical features of this apparently uncommon but important phenomenon. METHODS: We identified cases from the registries of relevant agencies and organizations, as well as newsmedia accounts, and developed a clinical profile of 25 children and young adults, 3 to 19 years of age. RESULTS: Each victim collapsed with cardiac arrest immediately after an unexpected blow to the chest, which was usually inflicted by a projectile (such as a baseball or hockey puck). Incidents took place during organized competitive sports in 16 cases and in recreational settings at home, at school, or on the playground in 9. In each instance, the impact to the chest was not judged to be extraordinary for the sport involved and did not appear to have sufficient force to cause death. Twelve victims collapsed virtually instantaneously on impact, whereas 13 remained conscious and physically active for a brief time before cardiac arrest. Cardiopulmonary resuscitation was administered within about three minutes to 19 victims, but normal cardiac rhythm could be restored in only 2 (both incurred irreversible brain damage and died shortly thereafter). Seven victims (28 percent) were wearing some form of protective chest padding. CONCLUSIONS: We speculate that most sudden deaths related to impact to the chest (not associated with traumatic injury) are due to ventricular dysrhythmia induced by an abrupt, blunt precordial blow, presumably delivered at an electrically vulnerable phase of ventricular excitability. This profile of blunt chest impact leading to cardiac arrest adds to our understanding of the range of causes of sudden death on the athletic field and may help in the development of preventive measures.

Adolescent↗