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PubMed1998

[Cardiovascular morbidity in children with human immunodeficiency virus infection].

UNLABELLED: Abnormalities of cardiovascular structure and function have been described among children with human immunodeficiency virus (HIV). In order to evaluate their occurrence and clinical predictors, 32 children infected with HIV, aged three months to 13 years (mean age = 3.11 +/- 3.51 years) were studied. Perinatal transmission was identified in 90% of the children. Twenty-two patients (pts) (69%) had symptoms, nine being moderately symptomatic and eight severely symptomatic. Fourteen pts had immunological disturbances and eight of them were severely immunosuppressed. Twenty-eight pts (88%) had HIV-1 infection and 6 recent Ebstein-Barr virus coinfection. Nineteen were on zidovudine and 14 on intravenous immunoglobulin treatment. Nineteen cardiovascular abnormalities were found in 15 pts (47%): 11 cases of pulmonary hypertension by echocardiographic criteria (eight of them had interstitial lung infiltrates seen on chest X-ray) and four cases of left ventricular dysfunction requiring anticongestive therapy. Other abnormalities were: patent ductus arteriosus, septal hypertrophy, mitral valve prolapse and pericardial effusion (one case each). Surface ECG displayed right ventricular hypertrophy in four pts, left ventricular hypertrophy in one patient and unspecific ST-T wave changes in two pts. Fourteen pts (44%) had sinus tachycardia with mean heart rate above the 95th percentile on 24-hour Holter monitoring. CONCLUSIONS: Cardiovascular abnormalities are frequent among children with HIV-1 infection in late stages; pulmonary hypertension is the most frequently found cardiovascular anomaly and seems to be related to either chronic or recurrent respiratory disease; cardiological follow-up is recommended for HIV-infected children.

AIDS-Related Opportunistic Infections↗
PubMed2006

Anemia and cardiovascular risk: the lesson of the CREATE Trial.

Anemia has received increasing attention as an independent cardiovascular risk factor in patients with chronic kidney disease (CKD); a number of studies have highlighted its clear relationship with CKD mortality, because its impact on cardiac function leads to the development of left ventricular hypertrophy. However, despite the association between higher hemoglobin levels and better outcomes, a number of clinical studies have failed to demonstrate that fully correcting anemia has a positive effect on morbidity and mortality in patients with CKD. The Cardiovascular Reduction Early Anemia Treatment Epoetin beta (CREATE) study was designed from the hypothesis that, as anemia develops early in the course of CKD and nearly at the same time as cardiovascular disease, its earlier correction may provide better protection against the development of cardiovascular abnormalities. This randomized, multicenter, open-label, parallel-group trial involved 603 patients who had moderate anemia (hemoglobin 11 to 12.5 g/dl) and stage 3 to 4 CKD (estimated GFR 15 to 35 ml/min) and were randomly assigned to attain complete or partial anemia correction. The final results are due to be published within a few months, but the preliminary analyses do not show that complete anemia correction leads to any cardiovascular advantage, although the cardiovascular event rate was half that expected, possibly as a result of patient selection, trial effect, and improved medical care. The baseline findings also indicated that the burden of cardiovascular disease already is very high even in relatively early stages of CKD.

Anemia↗
PubMed2006

Cardiovascular anomalies in patients with chromosome 22q11.2 deletion: a Korean multicenter study.

BACKGROUND AND OBJECTIVES: The 22q11.2 deletion syndrome is reported with increasing frequency worldwide, and its clinical manifestations, including cardiovascular anomalies, appear to be more diverse than previously reported. The aim of this study was to determine the incidence and the pattern of cardiovascular anomalies in Korean patients with 22q11 deletion. METHODS: This study involved six Korean institutions. We reviewed the clinical records of patients and confirmed the presence of 22q11.2 deletion by fluorescent in situ hybridization (FISH). RESULTS: A total of 222 patients were examined and 190 (85.6%) patients had the cardiovascular abnormalities: 63.2% tetralogy of Fallot (TOF), 20.5% isolated ventricular septal defects (VSDs), 5.3% interrupted aortic arch type B (IAA B), 3.6% double outlet right ventricle (DORV), 3.6% atrial septal defects (ASDs) and 1.7% truncus arteriosus (TA). Of 168 patients with VSD, 69.6% had the perimembranous type, 11.9% the total conal defect type, 6.5% the subarterial type, 4.2% the muscular type and 1.2% the mixed type. A right aortic arch was observed in 50% of patients, and an aberrant subclavian artery was significantly more common with a right (30.9%) than a left (18.3%) aortic arch (p<0.05). CONCLUSIONS: A wide variety of cardiovascular anomalies were present in Korean patients with the 22q11.2 deletion.

Abnormalities, Multiple↗
PubMed2000

Cardiac structure and function in fetuses of mothers infected with HIV: the prospective PCHIV multicenter study.

BACKGROUND: This study was designed to determine if vertically transmitted HIV infection and maternal infection with HIV are associated with altered cardiovascular structure and function in utero. METHODS: Fetal echocardiography was performed in 173 fetuses of 169 HIV-infected mothers (mean gestational age, 33.0 weeks; SD = 3.7 weeks) at 5 centers. Biparietal diameter, femur length, cardiovascular dimensions, and Doppler velocities through atrioventricular and semilunar valves and the umbilical artery were measured. Measurements were converted to z scores based on published normal data. RESULTS: Fetuses determined after birth to be HIV-infected had similar echocardiographic findings as fetuses later determined to be HIV-uninfected except for slightly smaller left ventricular diastolic dimensions (P =.01). The femur length (P =.03) was also smaller in the fetuses postnatally identified as HIV-infected. Differences in cardiovascular dimensions and Doppler velocities were identified between fetuses of HIV-infected women and previously published normal fetal data. The reason for the differences may be a result of maternal HIV infection, maternal risk factors, or selection bias in the external control data. CONCLUSIONS: Vertically transmitted HIV infection may be associated with reduced left ventricular size but not with altered cardiac function in utero. Fetuses of HIV-infected mothers may have abnormal cardiovascular structure and function and increased placental vascular resistance, regardless of whether the fetuses are subsequently found to be infected with HIV.

Adult↗
PubMed2006

The effects of exercise on haemodynamic function in relation to the familial hypertension risk model.

Offspring hypertensives are characterized by a hyperactive sympathetic nervous system and other early cardiovascular abnormalities that increase the risk of developing hypertension. A physically active lifestyle is associated with a lower risk of hypertension, although the mechanisms are incompletely understood and likely to be multifactorial. One aspect that has received little attention is the interaction of exercise with familial hypertension risk. The present review examines the effects of exercise on haemodynamic function in relation to the familial hypertension risk model. Paradoxically, exercise may be viewed as potent stressor to the cardiovascular system, although recent studies are beginning to show that cardiovascular adaptations, primarily mediated by changes in sympatho-vagal balance, following both acute and chronic exercise may be particularly important for individuals with familial risk of hypertension. Future studies that focus on inflammatory, metabolic, and genetic pathways may uncover further beneficial effects of exercise in relation to familial risk.

Adaptation, Physiological↗
PubMed1995

Role of transesophageal echocardiography in hemodynamically unstable patients.

OBJECTIVE: To evaluate the clinical impact of transesophageal echocardiography on subsequent management and outcome in hemodynamically unstable patients with suspected cardiovascular pathologic conditions. DESIGN: We reviewed data on patients with hemodynamic instability (hypotension, shock, or pulmonary edema) who underwent transesophageal echocardiography between December 1987 and May 1994. MATERIAL AND METHODS: A total of 127 patients (70 male and 57 female patients with a mean age of 68 years) underwent transesophageal echocardiography at our institution as part of the diagnostic procedures used to evaluate unstable hemodynamics. RESULTS: No clinically significant complication was encountered during the procedure; transesophageal echocardiographic imaging was inadequate in three patients (2%). Of the 124 patients with adequate images, transesophageal echocardiography disclosed a severe cardiovascular abnormality responsible for the unstable hemodynamics in 65 patients (52%), and 26 patients (21%) underwent urgent pericardiocentesis or a cardiac surgical procedure, primarily based on transesophageal echocardiographic findings. CONCLUSION: Transesophageal echocardiography can be safely performed in hemodynamically unstable patients, it produces a high diagnostic yield, and it provides important information for prompt therapeutic decision making. Therefore, we recommend transesophageal echocardiography as one of the initial diagnostic procedures in critically ill patients suspected of having an underlying cardiovascular disorder.

Aged↗
PubMed1995

Prenatal and presymptomatic diagnosis of the Marfan syndrome using fluorescence PCR and an automated sequencer.

The Marfan syndrome (MFS) is a heritable connective tissue disorder characterized by skeletal, ocular, and cardiovascular abnormalities. Defects in fibrillin, an elastin-associated microfibrillar protein, are now known to cause MFS. Since the discovery of fibrillin as the gene responsible for MFS, requests for prenatal and presymptomatic diagnosis have become common-place. Here we report the use of the polymerase chain reaction (PCR), using fluorescence labelled primers and an automated sequencer, to establish linkage data for 'molecular diagnosis'. The mistaken clinical diagnosis of MFS based on the appearance of a common cardiovascular manifestation, mitral valve prolapse, and a positive family history is also discussed.

Autoanalysis↗
PubMed1999

Roles for the winged helix transcription factors MF1 and MFH1 in cardiovascular development revealed by nonallelic noncomplementation of null alleles.

The murine Mf1 and Mfh1 genes have overlapping patterns of expression in the embryo and encode forkhead/winged helix transcription factors with virtually identical DNA binding domains. Previous studies have shown that Mfh1 null mutants have severe cardiovascular defects, including interruptions and coarctations of the aortic arch and ventricular septal defects (Iida et al., Development 124, 4627-4638, 1997). Here, we show that Mf1(lacZ) homozygous null mutants also have a similar spectrum of cardiovascular abnormalities. Moreover, most embryos doubly heterozygous for Mfh1(tm1) and Mf1(lacZ) die before birth with interruptions and coarctations of the aortic arch, dysgenesis of the aortic and pulmonary valves, ventricular septal defects, and other cardiac anomalies. This nonallelic noncomplementation and the similar patterns of expression of the two genes in the mesenchyme and endothelial cells of the branchial arches, outflow tract, and heart suggest that Mf1 and Mfh1 play interactive roles in the morphogenesis of the cardiovascular system. Implications for the development of human congenital heart defects are discussed.

Alleles↗
PubMed1983

Hypertrophic cardiomyopathy: a common cause of sudden death in the young competitive athlete.

The causes of sudden, unexpected death in highly-conditioned competitive athletes are summarized. In the vast majority of young athletes (less than 35 years of age) sudden death is due to underlying structural cardiovascular disease. Hypertrophic cardiomyopathy appears to be the most common cause of such deaths and may account for about one-half of the sudden deaths in a youthful athletic population. Cardiovascular abnormalities that appear to be less frequent important causes of sudden death include anomalous origin of the left coronary artery from the anterior sinus of Valsalva, ruptured aorta (due to cystic medial necrosis), idiopathic concentric left ventricular hypertrophy and coronary artery atherosclerosis. Other diseases which are probably particularly uncommon causes of sudden death in the young athlete include mitral valve prolapse, aortic valvular stenosis, acute myocarditis, QT interval prolongation syndromes, hypoplasia of the coronary arteries or sarcoidosis. Cardiovascular disease in young athletes is usually unsuspected during life. In only about 25% of those competitive athletes who die suddenly is underlying disease identified prior to participation and rarely is the correct clinical diagnosis made. In contrast, when sudden death occurs in older competitive or recreational athletes (over 35 years of age) it is usually due to coronary artery disease.

Adolescent↗
PubMed1999

Dermatosis and associated systemic signs in a cat with thymoma and recently treated with an imidacloprid preparation.

A cat was presented with acute-onset exfoliative erythroderma and gross and histopathological lesions of erythema multiforme. Marked cardiovascular abnormalities including heart failure occurred concurrently and a dermatogenic enteropathy was also seen. Medical treatment resolved the dermatopathy and enteropathy but the heart failure progressed. A drug reaction was initially suspected to be the underlying cause with no neoplasia being detected, but repeat radiographs subsequently revealed a thymoma which had not been visible on the initial radiographs. The dermatopathy may have been a paraneoplastic disease associated with thymoma and, possibly, exacerbated by a drug reaction to imidacloprid. The cardiovascular and gastroenterological diseases were thought to be systemic effects associated with the exfoliative erythroderma. The thymoma was surgically removed but the cat subsequently died from heart failure.

Animals↗
PubMed1982

Inheritance of mitral valve prolapse: effect of age and sex on gene expression.

To ascertain if mitral valve prolapse is inherited we studied 45 probands and 179 first-degree relatives. Echocardiographic mitral prolapse was present in 54 of 179 first-degree relatives (30%); at least one first-degree relative was affected in 29 families, including members of two generations in 23 families. The number of affected persons in the 54 sibships fell within the range predicted for autosomal dominant inheritance. The familial prevalence of prolapse was similar whether or not the proband had characteristic symptoms, auscultatory abnormalities, electrocardiographic findings, thoracic bony abnormalities, or coexistent heart disease. Mitral prolapse occurred in 37 of 90 women (41%) but 17 of 89 men (19%; p less than 0.005), and in 51 of 143 adults (35%) but only 3 of 36 children aged 1 to 15 (p less than 0.005). Mitral valve prolapse is an inherited autosomal dominant condition irrespective of clinical findings, and the mitral prolapse gene shows age and sex dependent expression. Mitral valve prolapse appears to be the commonest mendelian cardiovascular abnormality in humans.

Adolescent↗
PubMed2003

[Course of pregnancy, delivery and puerperium in women with Marfan syndrome].

Obstetric course and neonatal outcome in women with Marfan syndrome is the aim of numerous analyses. It is well known that pregnancies complicated by Marfan syndrome increase the risk of maternal morbidity and premature mortality. The main cause of this is cardiovascular abnormalities (aortic root dilatation, aortic dissection, rupture of the aorta, other cardiac abnormalities). We have presented a case history of a pregnant woman with a Marfan syndrome and the review of the literature.

Cesarean Section↗
PubMed2004

Neonatal blood pressure regulation.

Hypertension is often viewed solely as a disease of the adult. However, early indicators of hypertension are frequently observed in young children and neonates. Having an adequate appreciation of the normal range of infant blood pressure is critical for the appropriate management of the conditions associated with elevated or abnormally low blood pressure. In healthy neonates, systolic blood pressure increases rapidly during the first 6 weeks of life with the most rapid rise observed during the first 5 days. A similar pattern is observed for diastolic pressures. The observed increases in blood pressure are positively correlated with birth weight and both gestational and postnatal age. The incidence of hypertension in the neonate has been reported to range from 0.2% to 2.6% and is frequently an indicator of other renal or cardiovascular abnormalities. Systemic hypotension is reported in 24% to 45% of very low birth weight infants and is frequently caused by hypovolemia. The regulation of blood pressure is complex and the mechanisms involved remain to be fully elucidated. The results of several investigations into the molecular mechanism(s) of hypertension are considered.

Aging↗
PubMed2002

Autosomal dominant polycystic kidney disease - clinical and genetic aspects.

Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common inherited disorders in humans. It accounts for 8-10% of the cases of end-stage renal disease worldwide, thus representing a serious medical, economical and social problem. ADPKD is in fact a systemic disorder, characterized with the development of cysts in the ductal organs (mainly the kidneys and the liver), also with gastrointestinal and cardiovascular abnormalities. In the last decade there was significant progress in uncovering the genetic foundations and in understanding of the pathogenic mechanisms leading to the renal impairment. This review will retrace the current knowledge about the epidemiology, pathogenesis, genetics, genetic and clinical heterogeneity, diagnostics and treatment of ADPKD.

Animals↗
PubMed1999

Favorable life-style modification and attenuation of cardiovascular risk factors.

In order to develop an effective counseling system for prevention of cardiovascular diseases, the association of a favorably changed life-style with improved risk factors was examined. Participants were 7,321 office workers aged 30-69 years from in and around Nagoya city. The age-adjusted odds ratio (OR) and its 95% confidence interval (CI) were calculated to assess the likelihood of risk factor improvement by favorable life-style modifications during a 3-year period. Those who began to eat breakfast and increased their vegetable intake normalized their previously abnormal diastolic blood pressure with more than twice the likelihood (adjusted OR [95% CI] 2.89 [1.29-6.46] and 2.60 [1.18-5.75], respectively). 'Began to eat breakfast' was also significantly associated with normalized total cholesterol (TC) (1.84, [1.05-3.21]). 'Stopped eating till full' significantly normalized the body mass index (2.03; [1.25-3.28]), uric acid (1.65; [1.07-2.52]) and TC (1.43; [1.04-1.97]). Those who started regular exercise significantly normalized their high-density lipoprotein-cholesterol (HDL-C) abnormality with 1.69-times the likelihood (1.69; [1.24-2.29]) and those who began to walk briskly also improved their TC abnormality (1.85; [1.19-2.89]). HDL-C was normalized with 2.55-times the likelihood in those who quit smoking (2.55; [1.68-3.86]). Because favorable life-style modifications can attenuate abnormal cardiovascular risk factors, then proper advice on specific risk factors should be routinely given at each health check-up in order to prevent the onset of cardiovascular diseases in subsequent years.

Adult↗
PubMed2003

Left ventricular hypertrophy is a common echocardiographic abnormality in severe obstructive sleep apnea and reverses with nasal continuous positive airway pressure.

STUDY OBJECTIVES: To determine cardiac structural abnormalities by echocardiography in subjects with severe obstructive sleep apnea (OSA), and to determine the long-term effects of nasal continuous positive airway pressure (CPAP) on such abnormalities. DESIGN: Polysomnography was conducted on oximetry-screened patients who showed a desaturation index > 40/h and > or = 20% cumulative time spent below 90%. From these, 25 patients with severe OSA but without daytime hypoxemia underwent echocardiography prior to, then 1 month and 6 months following initiation of CPAP treatment. SETTING: Outpatient sleep disorders center. RESULTS: Of the 25 patients, 13 patients (52%) had hypertension by history or on physical examination. Baseline echocardiograms showed that severe OSA was associated with numerous cardiovascular abnormalities, including left ventricular hypertrophy (LVH) [88%], left atrial enlargement (LAE) [64%], right atrial enlargement (RAE) [48%], and right ventricular hypertrophy (16%). In all patients (intent to treat) as well as those patients compliant with CPAP therapy (84% > 3 h nightly), there was a significant reduction in LVH after 6 months of CPAP therapy as measured by interventricular septal distance (baseline diastolic mean, 13.0 mm; 6-month mean after CPAP, 12.3 mm; p < 0.02). RAE and LAE were unchanged after CPAP therapy. CONCLUSIONS: LVH was present in high frequency in subjects with severe OSA and regressed after 6 months of nasal CPAP therapy.

Adult↗
PubMed1984

The development of two subnuclei of the nucleus tractus solitarius in spontaneously hypertensive rats.

Changes in relative metabolic requirements and neuronal densities in the nucleus commissuralis (NC) and nucleus medialis (NM) of the nucleus tractus solitarius were studied in spontaneously hypertensive rats (SHR) during development. The changes in relative metabolic requirements in the two subnuclei of SHR between 2 and 12 weeks of age were similar to those previously reported for normotensive WKY at the same ages. However, the relative metabolic activity in the NC of 2- and 4-week SHR was significantly higher than in normotensive rats. The differences in metabolic requirements of the NC could not be explained by differences in the neuronal densities of this subnucleus in young SHR and may reflect abnormalities in developmental or functional activities in the pre-hypertensive rat. Neuronal densities in the NC of 8- and 12-week SHR and in the NM of 4-, 8- and 12-week SHR were significantly higher than in WKY controls. Differences in the neuronal densities in the NC and NM of SHR may be explained by a smaller brain size characteristic of this strain, but differences in the NC of SHR suggest that the alterations may underlie or result from the cardiovascular abnormalities associated with the spontaneous hypertension of this strain.

Animals↗
PubMed2002

Spontaneous spinal cerebrospinal fluid leaks and minor skeletal features of Marfan syndrome: a microfibrillopathy.

OBJECT: Spontaneous spinal cerebrospinal fluid (CSF) leaks are increasingly recognized as a cause of postural headaches. The authors examined a group of patients suffering from spontaneous spinal CSF leaks who also had minor skeletal features of Marfan syndrome for abnormalities of fibrillin-containing microfibrils. METHODS: Patients with spontaneous CSF leaks were evaluated for the clinical characteristics of connective tissue disorders. Skin biopsies were obtained in three patients with skeletal manifestations that constitute part of the Marfan syndrome phenotype. Cultured fibroblasts were studied for fibrillin-1 synthesis and incorporation into the extracellular matrix (ECM) by performing quantitative metabolic labeling and immunohistochemical analysis. Among 20 consecutive patients found to have spinal CSF leaks, four (20%) exhibited minor skeletal features of Marfan syndrome, but lacked any ocular or cardiovascular abnormalities. The mean age of these patients (30 years) was lower than that of the 16 patients without skeletal abnormalities (44 years; p = 0.01). Abnormalities in fibrillin-1 metabolism and immunostaining were detected in all three patients with the skeletal abnormalities who underwent examination, but not in a control patient without these skeletal manifestations. CONCLUSIONS: Twenty percent of patients who experience spontaneous spinal CSF leaks have minor skeletal features of Marfan syndrome. The authors demonstrated abnormalities in fibrillin-1 protein deposition in all patients examined, but only one person was found to have a fibrillin-1 abnormality typically found in classic Marfan syndrome. The results indicate that there is a heterogeneous involvement of other components of ECM microfibrils at the basis of this cerebrospinal manifestation. In addition, the authors identified a connective-tissue etiological factor in a group of disorders not previously classified as such.

Adult↗