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Results for “Cardiovascular Abnormalities”

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At least 73 records · Page 4Linked to original sources
PubMed2003

Cardiovascular abnormalities associated with the Stuve-Wiedemann syndrome.

The Stuve-Wiedemann syndrome (SWS) is a congenital bone dysplasia characterized by camptodactyly with ulnar deviation and congenital bowing of the long bones. Affected patients present with respiratory difficulties in the neonatal period or later and recurrent episodes of hyperthermia. The typical radiological findings are bowing of the long bones of the lower limbs, wide metaphyses with decreased density, and abnormal trabecular pattern. Generally, respiratory insufficiency and hyperthermia are reported to be the cause of death. We report on two sibs with SWS, who died from severe pulmonary hypertension with pulmonary artery wall abnormality. We suggest a common pathophysiological process, which could explain the cardiovascular findings that we observed immediately after birth in the two affected sibs. We hypothesize that the severe pulmonary hypertension due to the arterial wall abnormality could explain the neonatal death of these two children.

Bone and Bones↗
PubMed2005

Cardiovascular abnormalities and arrhythmias in patients with Ondine's curse (congenital central hypoventilation) syndrome.

Patients with congenital central hypoventilation syndrome (CCHS) (Ondine's curse syndrome) have impaired autonomic control of ventilation with intact voluntary control of respiration. Autonomic dysfunction and cardiac abnormalities are common in CCHS. Bradyarrhythmias are life-threatening and often require pacemaker insertion. We presented a case of a patient with CCHS suffering from long sinus pauses requiring cardiac pacemaker insertion. Patients with CCHS are at risk for pulmonary hypertension and cor pulmonale secondary to chronic hypoxia. Diaphragmatic pacing has been beneficial in some patients with CCHS. In this article, we review concomitant cardiac abnormalities and the occurrence of bradyarrhythmias in patients with CCHS.

Arrhythmias, Cardiac↗
PubMed1997

[Cardiovascular abnormalities in Bavaria 1984-1991].

The study presents data on cardiovascular malformations in Bavarian livebirths, born between 1984 and 1991. Cases have been ascertained retrospectively by reviewing hospital records of all children being referred to a children's hospital up to 2 years of age. The classification scheme was based on abnormalities in developmental mechanisms. Among 984,570 livebirths, 7020 cases with structural congenital heart disease were identified. The birth prevalence was 7.1 per 1000 livebirths. Between 1984 and 1991, total prevalence increased from 5.9/10(3) to 8.0/10(3). Prevalence in males was 7.3/10(3) and in females 6.9/10(3). 78.1% of all heart defects were isolated, the remaining 21.9% were associated either with chromosomal abnormalities (9.6%), non-chromosomal syndromes (1.0%), or noncardiac malformations of other organ systems (11.3%). Total fatality rate was 12.0%, with two thirds of deaths occurring within a month of birth or the following month of life. Data were compared with those of the Baltimore-Washington Infant Study. This study presents for the first time regional data on birth prevalences of congenital heart defects in Germany. The classification scheme reduces the wide spectrum of phenotype cardiovascular defects to several pathogenetic groups. The defects in each group may be related to similar causal factors.

Child, Preschool↗
PubMed2000

The influence of renal and cardiovascular abnormalities on blood pressure in Turner syndrome.

INTRODUCTION: Patients with Turner syndrome (TS) are at an increased risk of morbidity and mortality from cardiovascular disease. This study was undertaken to establish the prevalence of hypertension in patients with TS and to establish to what extent cardiovascular or renal abnormalities contribute to the measured blood pressure. PATIENTS AND METHODS: 62 patients with TS, age 5.4-22.4 years, had 24 h-ABPM (ambulatory blood pressure monitoring), echocardiography, renal imaging and measurement of recumbent plasma renin activity (PRA). Blood pressure was compared with population standards. RESULTS: 21% of the TS study population had mean systolic and 17% mean diastolic 24 h-ABPM measurements above the 95th percentile for age and sex (i.e. mild hypertension). Borderline blood pressure (i.e. 90th to 95th percentile) was found in another 17% of the patients. 57% of the patients had a blunted (i.e. less than 10%) fall in the night-time blood pressure. 24% of the patients had a detectable cardiac abnormality, 42% a detectable renal abnormality and 52% were found to have raised plasma renin activity. The presence of a cardiac or renal abnormality had no significant effect on blood pressure. Blood pressure of patients on growth and/or pubertal therapy was not different from those patients on no such treatment. CONCLUSION: Over 30% of patients with Turner syndrome were found to be mildly hypertensive and over 50% had an abnormal diurnal blood pressure profile. In this study we were unable to demonstrate that the presence of renal or cardiac abnormalities had an effect on recorded blood pressure. The use of growth hormone and oestrogen to manage growth failure and pubertal delay did not seem to affect blood pressure. This study suggests that there is a high prevalence of raised blood pressure in Turner syndrome patients. The 24 h-ambulatory blood pressure monitoring profile suggests that this may be secondary in origin, but we were unable to demonstrate an underlying mechanism with the renal and cardiac investigations performed.

Adolescent↗
PubMed2003

Does the kinin system mediate in cardiovascular abnormalities? An overview.

All the components of the kallikrein-kinin system are located in the cardiac muscle, and its deficiency may lead to cardiac dysfunction. In recent years, numerous observations obtained from clinical and experimental models of diabetes, hypertension, cardiac failure, ischemia, myocardial infarction, and left ventricular hypertrophy have suggested that the reduced activity of the local kallikrein-kinin system may be instrumental for the induction of cardiovascular-related diseases. The cardioprotective property of the angiotensin-converting enzyme inhibitors is primarily mediated via the kinin-releasing pathway, which may cause regression of left ventricular hypertrophy in hypertensive situations. The ability of kallikrein gene delivery to produce a wide spectrum of beneficial effects makes it an excellent candidate in treating hypertension and cardiovascular and renal diseases. In addition, stable kinin agonists may also be available in the future as therapeutic agents for cardiovascular and renal disorders.

Animals↗