[Embryology, etiology and pathogenesis of cardiovascular abnormalities].
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Congenital heart diseases have been studied much more extensively in children than in neonates. In this study, we report on the findings from 57 neonates seen from June of 1995 through June 1996 in the nursery of a large public hospital in Belém, Pará, Brazil. All were routinely examined by a paediatrician just after birth, and, when indicated, these babies were referred to the cardiology unit of our Hospital for assessment by a paediatric cardiologist. Most of the diagnoses were made by means of Doppler and cross-sectional echocardiography with color flow mapping. Several abnormalities of the cardiovascular system were diagnosed. The most frequent was patency of the arterial duct. But, since many ducts closed spontaneously, ventricular septal defect was the most frequent lesion seen even in the nursery. Four defects (patent arterial duct, ventricular septal defect, atrial septal defect and pulmonary stenosis) together accounted for two thirds of all cardiac abnormalities. Associated non-cardiac anomalies were more frequent in those with simple lesions within the heart. All the babies with complex heart disease, and the majority of those designated as having significant lesions, died before they could be discharged. Several risk factors were investigated. Among maternal drugs, misoprostol emerged as having a possible teratogenic effect.
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UNLABELLED: Marfan syndrome is an inherited disorder of connective tissue with manifestations in various organ-systems including cardiovascular system. The aim of this study was to characterize and determine the frequency of cardiovascular alterations by echocardiography in 2 age cohorts of Mexican patients with Marfan syndrome and their comparisons with control groups. MATERIAL AND METHODS: Sixty six with Marfan syndrome and 33 control patients were evaluated by echocardiography. Segments of the aorta and pulmonary artery were measured at different levels, cardiac valves were examined for prolapse and the interatrial septum was assessed for septal aneurysm. Numeric values were corrected for the body surface area and compared with the control group. RESULTS: Mean significant values between group I (children) and Group II (adults) were as follows: aortic annulus 16.62 +/- 4.57 mm/m2 vs 12.81 +/- 1.95 (p < 0.001), aortic root 23.30 +/- 7.49 mm/m2 vs 18.36 +/- 2.97 (p < 0.001), sinuses of Valsalva 24.14 +/- 7.29 mm/m2 vs 19.84 +/- 3.59 (p < 0.001), ascending aorta 18.43 +/- 5.90 mm/m2 vs 17.02 +/- 4.79 (p < 0.001), aortic arch 16.12 +/- 4.73 mm/m2 vs 14.20 +/- 2.68 (p < 0.001). Pulmonary valve prolapse was seen in 10/22 (45.5%) vs 7/44 (15.9%), p < or = 0.03. Interatrial septal aneurysm was found in 3/22 (13.6%) vs 20/44 (45.5%), p < or = 0.03. There was a significative diference in the presence of atrial septal aneurysm between the adult group and control group (p < 0.001). CONCLUSIONS: The incidence of cardiovascular abnormalities in our series is similar to that in the literature with the exception of the very high incidence of pulmonary valve prolapse vs control groups, then it suggests that the clinical manifestations of MFS are strikingly severe in the Mexican population. Also a high incidence of interatrial septal aneurysm (34.9%) in comparison to control groups (18.2%) was found.
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This study utilized a historical cohort to examine the relationship between maternal cocaine use during pregnancy and the occurrence of congenital cardiovascular abnormalities. All neonatal drug screens performed at Boston City Hospital during an 18-month period were reviewed (n = 554); for 214 (39%) screened high-risk neonates, results of toxicologic screens were positive for cocaine, and 340 (61%) neonates had no detectable cocaine. We compared the occurrence of cardiovascular malformations and electrocardiographic abnormalities in these two groups. Matches were sought between these 554 infants and our pediatric cardiology data base, which consisted of inpatient consultation, outpatient consultation, and electrocardiography. Forty-nine patients had drug screens and were also entered into our cardiology data base: 25 had both consultations and electrocardiograms, and 24 had electrocardiograms only. The rate of cardiac anomalies among the cocaine-positive infants was significantly higher (relative risk = 3.7; 95% confidence interval: (1.4, 9.4)) than the rate of these anomalies among the cocaine-negative comparison group (65/100 vs 18/1000); the rate for cocaine-positive infants was also significantly higher than published rates for general populations of infants. Several electrocardiographic abnormalities, high-grade ventricular ectopy, and cardiorespiratory arrests were also noted in our study population. We conclude that cocaine exposure during prenatal life appears to predispose infants to structural cardiovascular malformations, electrocardiographic abnormalities, and, possibly, cardiopulmonary autonomic dysfunction.
Using five non-invasive tests, abnormalities of cardiovascular reflex function were found in 20 of 50 patients with gastro-oesophageal reflux. Abnormalities of pupil cycle time, an index of non-vagal parasympathetic function, were found in only a few patients, implying that the cardiovascular abnormalities observed were not part of a generalised parasympathetic defect. The findings are consistent with the hypothesis that an abnormality of vagal function may contribute to the pathogenesis of gastro-oesophageal reflux.
The frequency of cardiovascular abnormalities was evaluated in 71 consecutive patients with acute injury to the spinal cord. Persistent bradycardia was universal in all 31 patients with severe cervical cord injury and less common in milder cervical injury (6 of 17) or thoracolumbar injury (3 of 23) (p less than 0.00001). Marked sinus slowing (71 versus 12 versus 4%, respectively, p less than 0.00001), hypotension (68 versus 0 versus 0%, p less than 0.00001), supraventricular arrhythmias (19 versus 6 versus 0%, p = 0.05) and primary cardiac arrest (16 versus 0 versus 0%, p less than 0.05) were significantly more frequent in the severe cervical injury group. The frequency of bradyarrhythmias peaked on day 4 after injury and gradually declined thereafter. All observed abnormalities resolved spontaneously within 2 to 6 weeks. The primary mechanism underlying these observations appears to involve the acute autonomic imbalance created by the disruption of sympathetic pathways located in the cervical cord. Acute severe injury to the cervical spinal cord is regularly accompanied by arrhythmias and hemodynamic abnormalities not found with thoracolumbar cord trauma. These abnormalities are limited to the first 14 days after injury, a period in which life-threatening disturbances must be anticipated.
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PURPOSE: We investigated the prevalence and clinical importance of cardiovascular abnormalities in patients with hyperthyroidism. METHODS: All consecutive patients diagnosed with hyperthyroidism during a period of 24 months were included in the study. Medical history, complete physical examination results, electrocardiographic findings, laboratory determinations, and Doppler echocardiographic findings were obtained for all patients within 24 hours of diagnosis, and after euthyroidism had been achieved. Age- and sex-matched controls also were studied. RESULTS: Thirty-nine patients (mean [+/-SD] age, 52 +/- 20 years; range, 25 to 86 years; 72% women), and 39 age- and sex-matched controls, were included. Atrial fibrillation was present in 7 patients (18%). Moderate or severe mitral or tricuspid regurgitation, or both, were present in 9 patients (23%) and in only 1 control (3%; P= 0.01). Mean pulmonary arterial systolic pressure was 38 +/- 12 mm Hg (range, 17 to 64 mm Hg) in patients and 27 +/- 4 mm Hg (range, 19 to 37 mm Hg) in controls (P= 0.001). Sixteen patients (41%) and 1 control (3%) had pulmonary arterial systolic pressure >or=35 mm Hg. Left ventricular systolic dysfunction was detected in 1 patient. After correction of hyperthyroidism, a significant decrease in pulmonary arterial systolic pressure was observed, and the levels became similar to those of controls. CONCLUSION: In patients with hyperthyroidism, there is a high prevalence of pulmonary hypertension and atrioventricular valve regurgitation. These abnormalities usually correct after treatment for hyperthyroidism.
Treatment for X-linked hypophosphatemia (XLH; vitamin D metabolites and phosphate salts) may result in hypercalcemia, hypercalciuria, nephrocalcinosis, and hyperparathyroidism. Cardiovascular abnormalities occur in association with these complications, but have not been reported in XLH. We hypothesized that such abnormalities may occur in XLH and evaluated cardiovascular status in 13 patients with this disease. All patients were asymptomatic and had normal cardiovascular physical examinations and Holter studies. Serum calcium and creatinine clearance were normal in all. However, all patients had mild to moderate nephrocalcinosis. Left ventricular hypertrophy was diagnosed by electrocardiogram in three and by ultrasonography in seven children. Baseline blood pressure (BP) was normal (mean +/- SD, 116 +/- 15/74 +/- 6 mm Hg). During exercise stress testing, systolic BP increased in all patients, but the maximal systolic pressure was less than that in healthy age- and sex-matched controls (156 +/- 20 vs. 175 +/- 23; P = 0.002, by t test). An abnormal increase in diastolic BP occurred at all levels of work load in XLH patients; their peak exercise diastolic BP was 91 +/- 12 vs. 72 +/- 6 mm Hg in controls (P < 0.0001, by t test). Whether these abnormal findings are primary defects in XLH or represent complications of treatment is unclear. Patients with XLH should be monitored closely for the development of hypertension and left ventricular hypertrophy. Investigation of the mechanisms involved and establishment of therapeutic guidelines are indicated.
Cardiovascular and ECG abnormalities were studied following injection of venom of Buthus tamulus, a common scorpion found in South India. Venom was administered in doses of 2 and 4 mg/kg body weight. Subsequent estimation of glycogen content of different chambers of the heart, showed a significant reduction in tissue glycogen levels in both atria and ventricles in animals treated with a venom dose of 2 mg/kg. However, a significant reduction occurred only in atria with a higher venom dose of 4 mg/kg.
This review is an attempt to highlight evidence that may implicate the cardiovascular abnormalities in the pathogenesis of hypertension. Many physiological, pharmacological, and biochemical studies have been conducted in in vitro and in vivo systems. Since blood pressure can rise in response to an increase in cardiac output and/or a rise in peripheral resistance, abnormalities may be present in one or more of the multiple factors that affect these two parameters in hypertension. These multiple factors include various neurohumoral factors. Increased levels of various vasoconstrictor neurohumoral factors have been found in patients with hypertension. Vasoconstrictor neurohumoral factors such as catecholamines, angiotensin II, and endothelin-1 induce vascular smooth muscle cells(VSMCs) proliferation and contraction. On the other hand, vasodilator neurohumoral factors such as natriuretic peptides and adrenomedulin inhibit VSMCs proliferation. Both neurohumoral factors mutually interact and develop hypertension.
Tissue kallikrein is a serine protease thought to be involved in the generation of bioactive peptide kinins in many organs like the kidneys, colon, salivary glands, pancreas, and blood vessels. Low renal synthesis and urinary excretion of tissue kallikrein have been repeatedly linked to hypertension in animals and humans, but the exact role of the protease in cardiovascular function has not been established largely because of the lack of specific inhibitors. This study demonstrates that mice lacking tissue kallikrein are unable to generate significant levels of kinins in most tissues and develop cardiovascular abnormalities early in adulthood despite normal blood pressure. The heart exhibits septum and posterior wall thinning and a tendency to dilatation resulting in reduced left ventricular mass. Cardiac function estimated in vivo and in vitro is decreased both under basal conditions and in response to beta-adrenergic stimulation. Furthermore, flow-induced vasodilatation is impaired in isolated perfused carotid arteries, which express, like the heart, low levels of the protease. These data show that tissue kallikrein is the main kinin-generating enzyme in vivo and that a functional kallikrein-kinin system is necessary for normal cardiac and arterial function in the mouse. They suggest that the kallikrein-kinin system could be involved in the development or progression of cardiovascular diseases.
The accuracy of conventional methods of assessing the periradicular tissues, especially important in the case of a patient with cardiovascular abnormality, is questioned. The results of histological assessment in 81 teeth are reported. The ideal of a biological obturation of the root canal is emphasized.
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