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It has been suggested by several authors that the prevalence of mitral valve prolapse and aortic root dilation is increased in individuals with the fragile X syndrome. The prevalence of these abnormalities in young children with fragile X has not been established. Sixteen boys and 1 girl 13 years or younger were studied. Only 1 child (6%) had the typical examination findings of mitral valve prolapse, although his echocardiogram was normal. From this study it appears that cardiac abnormalities in fragile X syndrome develop in late childhood and adolescence. It seems important to follow these children carefully so that these cardiac abnormalities can be documented when they do develop.
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Costello syndrome is characterized by mental retardation, loose skin, coarse facies, skeletal abnormalities, cardiovascular abnormalities (congenital heart defects, cardiomyopathy, rhythm disturbances), and predisposition to neoplasia. Endocrine abnormalities including growth hormone deficiency, adrenal insufficiency, glucose intolerance, parathyroid adenoma with hyperprolactinemia and hypoglycemia have been described. Hypoglycemia has been documented due to growth hormone and cortisol deficiency. We report on two patients with Costello syndrome and persistent hyperinsulinemic hypoglycemia and review the endocrine manifestations of Costello syndrome. Both patients required diazoxide therapy to stop the unregulated insulin secretion and maintain normoglycemia. The mechanism of persistent hyperinsulinism in patients with Costello syndrome is unclear.
Major congenital malformations, many of which result from abnormal cardiovascular patterning, remain the leading cause in infant mortality and morbidity. Targeted mutations of several genes (including VEGF and VEGF receptors) and certain teratogenic agents (including excess alpha-D-glucose) give rise to embryonic lethal phenotypes associated with failure in the formation of a functional vitelline circulation and aberrant organogenesis. Our work to date has demonstrated that yolk sac vasculopathy and failure of endocardial cushion epithelial-mesenchymal transformation occurs in hyperglycemic conditions in murine whole conceptus culture and in embryos from streptozotocin-induced diabetic mice. These cardiovascular abnormalities are associated with changes in expression and phosphorylation state of adhesion molecules such as platelet endothelial growth factor-1 and expression of growth factors such as vascular endothelial growth factor (VEGF-A). Further understanding of the effects of maternal diabetes on yolk sac and embryonic vasculogenesis/angiogenesis and organogenesis may lead to novel approaches in treating and preventing major birth defects.
Sleep-disordered breathing is associated with chronic intermittent asphyxia and with a variety of cardiovascular abnormalities. Cardiovascular morbidity and mortality are linked to altered platelet function, and platelet function is affected in sleep-disordered breathing. As there is evidence that chronic continuous hypoxia may alter platelet number and function, the aim of the present study was to test the hypothesis that chronic intermittent asphyxia affects platelet count, activation and aggregation. Rats were treated with a hypercapnic hypoxic gas mixture (minimum of 6-8% O2, maximum of 10-14% CO2) for 15 s, twice per minute for 8 h per day for 3 weeks. Blood was analysed for platelet count, platelet activation (CD62p expression using flow cytometry), response to low dose ADP, haematocrit, red cell count and haemoglobin concentration. A platelet function analyser measured the closure time of an aperture, dependent on platelet aggregation. Compared to controls (n = 16), chronic intermittent asphyxia (n = 13) reduced body weight and increased right ventricular weight but had no significant effect on platelet count (control, 880.4 +/- 20.1; treated: 914.1 +/- 35.2 x 10(3) microl(-1); mean +/- S.E.M.), on the reduction in platelet count in response to ADP (control, reduced to 206.7 +/- 49.0; treated, reduced to 193.8 +/- 35.9 x 10(3) microl(-1)), or on the percentage of platelets positive for CD62p (control, 5.2 +/- 0.7; treated, 6.0 +/- 0.8%). Chronic intermittent asphyxia significantly (P = 0.037) reduced the closure time (control, 90.9 +/- 7.7; treated, 77.7 +/- 3.8 s), indicating greater adhesion and aggregation. There was no significant difference in haematocrit, red cell count and haemoglobin concentration. In conclusion, chronic intermittent asphyxia has no effect on platelet count but does increase platelet aggegation in rats. These data support the idea that chronic intermittent asphyxia alters platelet function in sleep-disordered breathing.
OBJECTIVE: To assess the usefulness of specific cardiovascular reflex tests in childhood and to estimate the prevalence of cardiovascular reflex abnormalities among children with IDDM. In adults, abnormal cardiovascular reflexes are a frequent complication of diabetes, associated with increased morbidity and mortality. RESEARCH DESIGN AND METHODS: We measured heart-rate responses to deep breathing and standing in ambulatory children with and without IDDM between 6-19 yr of age. A subgroup of the IDDM patients was retested after 1 yr. RESULTS: We found the best techniques for detecting cardiovascular reflex abnormality in children were as follows: to record heart-rate responses to deep breathing either as the change in heart rate corrected for inspiratory heart rate or as the ratio of R-R intervals during expiration and inspiration; and to use the Maximum-minimum ratio for heart-rate responses to standing. HR-DBc was lower in diabetic than nondiabetic children (28.6 +/- 9.2% [n = 248] vs. 33.6 +/- 6.8% [n = 60]; P < 0.0005). Similarly, E:I was lower in children with IDDM than control subjects (1.42 +/- 0.19 [n = 248] vs. 1.52 +/- 0.15 [n = 60]; P < 0.0005). In the IDDM group, 21% of the children had abnormal HR-DBc or E:I responses. HR-STND M/m was lower in children with IDDM than control subjects (1.28 +/- 0.20 [n = 167] vs. 1.38 +/- 0.22 [n = 45]; P < 0.014). Among children with IDDM, 11.4% had abnormal HR-STND M/m responses. Overall, 29% of IDDM children tested abnormal in either HR-DBc or HR-STND M/m; 3% were abnormal in both tests. We found no correlation of HbA1c levels (n = 74) or duration of diabetes with either HR-DB, expiration to inspiration (n = 248), or HR-STND M/m (n = 167). In patients who were reevaluated after 1 yr we found a high correlation of the first and repeat HR-DBc tests (r = 0.47, n = 75, P < 0.0001), E:I (r = 0.53, n = 75, P < 0.0001), and HR-STND M/m (r = .49, n = 37, P < 0.002), but no evidence of an increased number of children with cardiovascular reflex abnormality. CONCLUSIONS: With easily performed HR-DB and HR-STND tests, we detected cardiovascular reflex abnormality in 29% of children with IDDM. We found no correlation of changes in HR-DB and HR-STND with HbA1c or duration of diabetes. These tests provide an objective clinical measurement to monitor autonomic neuropathy in children with diabetes.
Noonan syndrome is the second most frequent congenital malformation syndrome, after Down syndrome, associated with cardiovascular abnormalities. The most prevalent cardiovascular abnormalities in Noonan syndrome are pulmonary stenosis and hypertrophic cardiomyopathy. We report the case of a 12-year-old girl with Noonan syndrome who had multiple cardiovascular abnormalities, including extensive bilateral coronary artery dilatation, valvular and supravalvular pulmonary stenosis, atrial septal defect, and mitral valve prolapse. Both coronary artery dilatation and supravalvular pulmonary stenosis, although rarely reported, are abnormalities of the cardiovascular system that may occur in Noonan syndrome.
BACKGROUND: It is unclear whether fibrinogen predicts cardiovascular events independently of echocardiographic cardiovascular abnormalities and traditional risk factors. METHODS: We studied 2671 American Indians who participated in the second Strong Heart Study examination (1993-1995) and were observed for an average of 50 +/- 6 months. Participants with baseline overt coronary artery disease or a plasma creatinine level > or =3 mg/dL were excluded. Left ventricular hypertrophy, elevated arterial stiffness, and subnormal myocardial contractility were assessed by echocardiography. RESULTS: Prevalences of echocardiographic abnormalities and cardiovascular event rates were higher with higher fibrinogen levels. Incident cardiovascular events (n = 158) and deaths (n = 64) were more frequent in participants with elevated fibrinogen levels (>400 mg/dL) than in participants with lower fibrinogen levels, as was the prevalence of echocardiographic abnormalities (both P <.01). Incident cardiovascular fatal and nonfatal events and cardiovascular deaths were 4 and 8 times higher, respectively, in participants with both elevated fibrinogen levels and echocardiographic abnormalities than in participants with neither echocardiographic abnormalities nor elevated fibrinogen levels. However, participants with fibrinogen levels >400 mg/dL had a 2 times greater relative risk of cardiovascular events or mortality, independent of both risk factors and echocardiographic abnormalities. CONCLUSIONS: In a population-based sample of adults without clinical evidence of coronary artery disease at baseline, fibrinogen levels predicted cardiovascular events independent of traditional risk factors, left ventricular hypertrophy, elevated arterial stiffness, and subnormal myocardial systolic function.
Both cardiovascular disturbances and fatigue are frequent in multiple sclerosis (MS). We investigated their relationship in 84 MS patients (mean age 39.9 +/- 8.9 years) using five established autonomic tests and three different fatigue questionnaires. 64.2% of the patients were categorised as being fatigued Fatigue perception was weakly related to EDSS. Moderate cardiovascular disturbances were found in 16.6% of the patients, and 10.7% had severe cardiovascular autonomic abnormalities. Cardiovascular dysfunction was slightly related to age and to EDSS. In 19.4% of all patients signs of autonomic failure and fatigue were co-existent Using correlation analysis, we found only weakly significant correlation coefficients between some single autonomic test parameters and fatigue scores, which were confounded by age effects. The analysis of dichotomised data revealed slightly significant differences in fatigue experience between patients with and without abnormalities regarding the handgrip test and the Valsalva reaction. Thus, autonomic disturbances might contribute to fatigue symptoms in a MS subgroup, but the overall influence of the autonomic cardiovascular regulation towards fatigue experience seems to be of minor relevance.
1. The effects of tenidap sodium and placebo on digoxin pharmacokinetics were compared in 14 healthy young men, in a double-blind, parallel-group study lasting for 24 days. 2. Subjects were administered digoxin alone for the first 10 days and digoxin plus tenidap 120 mg day-1 or placebo for the remaining 14 days. 3. Changes in the means between day 10 (digoxin monotherapy) and day 24 (combined therapy) for renal clearance, area under the plasma concentration-time curve during the dosing interval, and the minimum and maximum plasma digoxin concentrations did not differ significantly between the tenidap and placebo groups. There was a small but statistically significant increase (0.5 h) in the time taken to reach maximum plasma digoxin concentration following 14 days' continuous tenidap co-administration compared with placebo, but this was not considered to be clinically meaningful. 4. Co-administration of tenidap and digoxin was well tolerated. No subject withdrew from the study during combination treatment. Treatment-related adverse events were of mild to moderate severity and were reported by four subjects on digoxin monotherapy, four on tenidap and digoxin, and by two on digoxin and placebo. Those reported by the tenidap group predominantly affected the gastrointestinal system and were mild in severity. There were no reports of laboratory test abnormalities or cardiovascular abnormalities related to combined digoxin and tenidap administration. 5. The results of this study indicate that, in healthy young men, co-administration of tenidap with digoxin does not have any apparent clinically significant effects on the pharmacokinetic profile of digoxin, and the treatment is well tolerated.
OBJECTIVES: To provide the reader with an overview of the many causes of sudden cardiac death in young athletes and to present various strategies for preparticipation cardiovascular screening. DATA SOURCE: A MEDLINE search using the phrase sudden cardiac death and the key word athlete for the years 1980 to 2000. DATA SYNTHESIS: Sudden cardiac death is a rare event in athletics. More than 20 different causes have been described, but most cases result from a few distinct entities. Most afflicted athletes have no symptoms before death. Many attempts have been made to detect those at risk for sudden cardiac death before athletic participation. At this time, a thorough history and physical examination are the most efficient screening methods for detecting cardiovascular abnormalities. Studies show that the current status of preparticipation cardiovascular screening of high school and college athletes nationwide is poor. CONCLUSIONS AND RECOMMENDATIONS: The use of diagnostic tests to screen for cardiovascular abnormalities is ineffective and inefficient. The most prudent and effective methods of preparticipation screening for cardiovascular abnormalities at this time are a history and physical examination in accordance with the American Heart Association guidelines. Athletic trainers must ensure that their institutions comply with these minimum standards.
To determine whether patients with MS had abnormalities of autonomic cardiovascular functions, we evaluated 22 MS patients and 20 control subjects with a battery of six standardized tests. The two groups differed on three tests: heart rate and blood pressure responses to standing, and the cold-face test. One-half of the MS patients had abnormalities on two or more tests, but individual patients showed diverse abnormality patterns. Abnormalities of neural cardiovascular regulation are frequent in MS patients and show a heterogeneous pattern, consistent with scattered plaques.
As a physician, coach, or trainer, we see athletes as healthy, physically fit, and able to tolerate extremes of physical endurance. It seems improbable that such athletes may have, on occasion, underlying life-threatening cardiovascular abnormalities. Regular physical activity promulgates cardiovascular fitness and lowers the risk of cardiac disease. However, under intense physical exertion and with a substrate of significant cardiac disease--whether congenital or acquired--athletes may succumb to sudden cardiac death. The deaths of high-profile athletes receive much attention through the national news media, but there are also deaths of other athletes. With repetitive, intense physical exercise, the heart undergoes functional and morphologic changes. Knowledge of those changes may help one identify cardiovascular abnormalities that can cause sudden death from the heart known as an "athlete's heart." This article will review cardiovascular diseases that may limit an athlete's participation in sports and that may put an athlete at risk for sudden cardiac death. It also reviews the extent and limitations of the cardiovascular preparticipation screening examination. Team physicians, coaches, and trainers must understand the process of evaluation of a symptomatic athlete that may indicate significant cardiac abnormalities. Finally, guidelines to determine eligibility of athletes with cardiovascular disease to return to sports will be reviewed.