SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Polycystic ovary syndrome (PCOS) is not only a reproductive problem but a complex, endocrine, multifaceted disease with several health complications. Cardiovascular abnormalities represent important long-term sequelae of PCOS.
An excess of structural defects occurs in monozygotic twins compared in dizygotic twins or singletons. The excess is composed of three categories of defects. The first includes defects which are part of the MZ twinning, such as conjoined twins and some amorphous twins. In addition, all early embryonic malformations and malformation complexes such as sirenomelia mc. holoprosencephaly mc. and anencephaly mc are increased in MZ twins. The reason for this association is considered to be the common etiology for both the MZ twinning and the early malformation problem. MZ twins provide an excellent model for appreciating the spectra of particular malformation complexes, since the twins often have different gradations in severity of the same type of structural defect. The finding of both discordant and concordant MZ twins with Goldenhar, de Lange, and Rubinstein-Taybi syndromes suggests that these "syndromes" might be early malformation complexes. The other two categories are considered secondary to the MZ twinning process. The most unique category results from any vascular interchange between the MZ twins. Depending on their nature, vascular connections may give rise to reverse flow with acardiac status in one twin during early development, or to vascular disruptions from a deceased co-twin with intravascular coagulation causing embolization in the surviving co-twin. The latter defects may include microcephaly, porencephalic cysts, hydranencephaly, intestinal atresia, aplasia cutis, and limb amputation. Unequal growth may occur as a result of artery to vein placental anastomoses. The final category is deformations due to crowding in utero during late gestation. These do not differ from those in DZ twins.
Gap junctions are composed of connexin (Cx) proteins and mediate intercellular communication required for many developmental and physiological processes. Here we describe the isolation and characterization of Cx48.5, a zebrafish connexin with the highest sequence identity to mammalian Cx46. Expression analysis showed that Cx48.5 is expressed in the adult and embryonic lens and heart, adult testis, and transiently in the embryonic otic vesicles. Injection of Cx48.5 cRNA into Xenopus oocytes elicited intercellular electrical coupling with voltage sensitivity similar to mammalian Cx46. In single oocytes, Cx48.5 also induced large outward currents on depolarization, consistent with gap-junctional hemichannels. Disruption of Cx48.5 expression in embryos with antisense morpholino oligos (morpholinos) revealed that Cx48.5 has an essential role in the maintenance of lens homeostasis. The morpholino-treated embryos also developed small lenses and eyes as well as severe cardiovascular abnormalities.
The frequency of air embolism was studied in 21 patients during total hip replacement. Two groups were examined, one having femoral shaft cement insertion by hand, the other by Exeter cement gun. Venous air embolism was common throughout the hip surgery, but was especially so during prosthesis positioning in the femoral shaft. There were fewer air emboli and cardiovascular sequelae detected in the gun-inserted cement group, and the only patients to show clinically significant cardiovascular abnormalities during insertion of cement and prosthesis were those having cement insertion by hand. We conclude that the incidence of air embolism and associated cardiovascular changes during total hip replacement may be expected to be reduced in those patients in whom a cement gun is used to place the cement.
Explore the source record for details and available documents.
In the course of gestation, many bacteria, parasites, and viruses may infect the pregnant woman, but few cross the placenta to affect the fetus and fewer still affect the fetal heart. Although the incidence of fetal cardiac infection is low, the effect on the fetus is major. In terms of frequency, rubella virus, Toxoplasma gondii, and Coxsackie virus B are the principal infectious agents affecting the fetal heart, but any number of organisms may cross the placenta to affect the fetus. The pathogenesis of infection of the fetal heart relates to the agent and to the time of gestation when the infection occurs. The agent affects the heart along one or more of three separate pathways: inhibition of cell growth, cytolysis, and interference with the blood supply. Most agents cause cytolysis, stimulating inflammation and scarring. Although several agents carry the suspicion of teratogenicity, only rubella virus has been incriminated with certainty as capable of functioning along each of the three pathways with the potential to serve as teratogen.
Explore the source record for details and available documents.
1. This study was undertaken to determine whether, in a group of patients complaining of recurrent syncopal attacks but with no apparent cause, there was evidence of abnormal cardiovascular reflex control. 2. The steady-state responses of blood pressure, heart rate and cardiac output to head-up tilting were determined in 67 patients using entirely 'non-invasive' methods. In some patients we also studied the immediate response of pulse interval to carotid baroreceptor stimulation by neck suction. 3. Two of the patients developed vasovagal attacks during the 20 min test period of head-up tilting. Eighteen others showed postural hypotension, defined as a fall in blood pressure to outside the limits of two SDS from the mean values of age-related control subjects. 4. Patients who showed postural hypotension had a mean fall in cardiac output significantly larger than that in age-related control subjects. Responses in the nonhypotensive patients did not differ significantly from controls. 5. Stimulation of carotid baroreceptors resulted in significantly smaller responses of pulse interval in the patients defined as having postural hypotension compared with the non-hypotensive patients and with the age-related control subjects. 6. In some of the patients who did not show postural hypotension during the standard test, the duration of tilt was prolonged for up to 1 h. Five out of 26 patients developed vasovagal attacks. All the vasovagal patients showed an initial tachycardia and the response of pulse interval to neck suction was significantly larger than in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
The first autopsy case of dilated cardiomyopathy associated with Noonan's syndrome is described. A 9-month-old girl with Noonan's syndrome died from cardiac failure. Autopsy showed biatrial and biventricular enlargement of the heart. The posterior half of the ventricular septum and right ventricular wall were remarkably thin. Other parts of the wall were nearly normal in thickness, but both ventricular cavities were dilated. Microscopically, the myocardium of both ventricles consisted of mainly abnormally thinned, elongated, and loosely arranged myocardial fibers lacking immunoreactivity to anti-dystrophin antibody. Myocardial disarray was not found except for where it normally existed. The abnormal changes of the myocardial fibers were considered to be primary. Common cardiomyopathy associated with Noonan's syndrome is a hypertrophic type. Various types of cardiovascular abnormality associated with Noonan's syndrome, including dilated cardiomyopathy, might be disclosed by further investigation and precise diagnosis of Noonan's syndrome.
Even today, a restrictive attitude frequently leads the physician to discourage the patient with cardiovascular abnormalities from sojourning at an altitude over 1000 m. This attitude, however, is not supported by any scientific proof. After a review of the major cardiovascular adaptations during high altitude exposure, we reported the principal studies of the effects of high altitude on patients with coronary heart disease, particularly during exercise. On the basis of personal experience and of other authors, we can state that the patient with ischemic heart disease, asymptomatic and with a recent clinical and functional evaluation, can stay in the mountains, even at altitudes of 2000-3000 m, and can hike and ski (cross-country and downhill). The risks appear to be related to factors independent of altitude, such as excessive cold or intense emotional stress due to dangerous situations, conditions that must consequently be avoided. On the other hand, an individual approach should be followed for the other congenital and acquired heart diseases, in which case we must consider, in addition to the clinical situation, some peculiar aspects of mountain environment (hypoxia, isolation, difficult access to medical facilities). Finally, the hypertensive patient, expected to have higher blood pressure values, especially diastolic, should frequently record his values during the first week at high altitude, eventually adjusting the therapy.
The aim of this study has been to assess the prevalence of autonomic neuropathy among non-insulin dependent diabetic patients, and to determine whether a correlation could be found between autonomic impairment and the following: age, sex, duration of diabetes, body mass and metabolic control. Two hundred and twenty one non-insulin dependent patients were submitted to four cardiovascular tests: heart rate response to deep breathing and to standing up; blood pressure response to handgrip and to standing up. Sixty six percent of patients showed at least one abnormal cardiovascular response. The prevalence of autonomic impairment was higher in non-insulin dependent than in insulin-dependent diabetics. Patients were grouped according to the extent of autonomic impairment: absent (33.5%), early (27.6%), definite (3.6%), severe (4.5%). An atypical pattern (abnormality of blood pressure responses in absence of a definite abnormality of heart rate responses) was found in 30.8% of patients. Heart rate responses correlated significantly with age (p less than 0.001). No correlation between test results and duration was found in the multivariate analysis. The tests' results did not correlate with metabolic control or body mass index. Patients with symptoms of autonomic neuropathy had values for heart rate response to deep breathing and to standing significantly lower than those without (p less than 0.05).
OBJECTIVE: To systematically evaluate the recent literature regarding the relationship between childhood sleep-disordered breathing (SDB)/obstructive sleep apnoea (OSA) and cardiovascular diseases in children. METHODS: The literature about SDB/OSA and blood pressure, sympathetic activation, arterial distensibility, ventricular hypertrophy and insulin resistance were studied. Meta-analysis of risk of hypertension and high apnoea-hyponoea index were performed to calculate the combined odds ratio and it is equal to 2.93 (95% CI = 1.18-7.29). RESULTS: The results suggest a significant association between SDB/OSA and hypertension. However, the data are not adequate to draw firm conclusion although evidences were emerging to suggest that SDB/OSA affects blood pressure in either directions in children. Limited evidences also suggest that SDB/OSA is associated with increased sympathetic activation, decreased arterial distensibility and ventricular hypertrophy. CONCLUSIONS: There is now increasing but not adequate evidence that childhood SDB/OSA is associated with detectable cardiovascular abnormalities.
Although a variety of pharmacological agents have been used to treat patients with chronic fatigue syndrome none has been shown to effect a complete resolution of symptoms. Data obtained from a retrospective study and from an objective assessment of the aerobic work capacity of patients with this disorder suggest that the underlying pathophysiological abnormality is a disorder of sleep regulation. This results not only in profound fatigue and lethargy but also reduced sensory threshold for pain, disordered temperature regulation, cardiovascular abnormalities, disturbed higher cerebral function and mental depression. Drugs which modulate sleep, such as tricyclic antidepressants, have a limited effect in improving the symptoms that CFS patients experience. We suggest that other agents which affect central nervous system neurotransmitters, particularly serotonin, may have potential in the management of this condition and need to be evaluated in large controlled clinical trials.
A persistent left superior vena cava is an uncommon congenital abnormality. It arises when the left anterior cardinal vein fails to regress during the embryonic period. Although such patients are usually asymptomatic, they may have associated cardiovascular abnormalities. The anaesthetist may encounter difficulty in the insertion of pulmonary artery catheters. Other implications in the management of these patients in the operating theatre or intensive care unit are discussed.
Eight tests for cardiovascular reflex function were evaluated in a group of 140 diabetic patients. The sensitivity, reproducibility and normal values of each test were previously assessed in a group of 70 normal controls. The measure of the R-R interval variation during six cycles of deep breathing (expiration/inspiration ratio) proved to be the most sensitive test, and was selected for screening. The Valsalva ratio, the bradycardia/tachycardia ratio post-standing and the blood pressure response to standing and to sustained handgrip served as a confirmatory test of autonomic neuropathy and were related to the severity of the lesion. The R-R interval variation during one deep breathing cycle, the post-standing tachycardia, and the R-R 30/15 standing ratio proved to be of little or not value in assessing cardiovascular neuropathy. Cardiovascular autonomic neuropathy was diagnosed in 38.5% of our diabetic population, predominantly in patients with other clinical evidence of autonomic neuropathy. In a few asymptomatic patients, abnormal cardiovascular responses were the first evidence of autonomic lesion.
The aim of this report was to evaluate late left ventricular function in survivors of Wilms' tumor and to compare patients treated with anthracyclines with those treated without anthracycline and with normal subjects. Wilms' tumor survivors treated without anthracycline had no myocardial abnormalities. A large percentage of patients treated with anthracycline presented with increased end-systolic wall stress. Results indicate that there is a high incidence of subclinical cardiovascular abnormalities in such patients.
To evaluate the role of tumor necrosis factor-alpha (TNF-alpha) in hemodynamic alterations, multiple organ damage, and mortality caused by hemorrhagic shock, we employed a monoclonal antibody to TNF-alpha (TNF-alpha MAb) in anesthetized rats subjected to prolonged hemorrhagic shock (mean arterial pressure of 30-35 mmHg for 180 min) followed by resuscitation over 50 min. Treatment of rats with 20.0 mg/kg TNF-alpha MAb 15 min after the end of resuscitation significantly decreased the total peripheral resistance index (P = 0.031) and provided remarkable protection from multiple organ damage compared with controls. The 48-h survival rate was significantly higher in the treatment group (73.3%) than in the control group (26.7%; P = 0.029). The results suggest that TNF-alpha induced by hemorrhagic shock in rats is an important mediator of pathophysiological alterations associated with cardiovascular abnormalities, multiple organ injury, and even lethality. Postresuscitation treatment with TNF-alpha MAb, even after an initial TNF-alpha formation had occurred, significantly attenuated the cardiovascular consequences and improved the survival rate. Thus monoclonal antibodies to TNF-alpha might provide new prospects in the treatment of hemorrhage-related disorders.
The cardiovascular effects of tianeptine were assessed by a specific placebo-controlled trial in healthy volunteers and by heart rate, blood pressure and electrocardiogram data analyses in five studies enrolling depressed patients. In two of these studies the effects of tianeptine were compared to those of amitriptyline. The three other studies were performed as open, long-term trials (up to one-year treatment) in large populations of patients (more than 3,300 patients). The findings show that tianeptine does not modify heart rate, blood pressure, conduction or ventricular function. Tianeptine was well tolerated in depressed patients and induced no significant changes at the current dosage in treatment periods from three-months to one-year even in elderly patients, patients with cardiovascular abnormalities or alcoholic patients. Fewer cases of orthostatic hypotension were observed than with other antidepressants. Suicide attempts with tianeptine overdosage did not lead to death due to cardiovascular complications.