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PubMed1979

Echocardiographic abnormalities in patients with cystic fibrosis.

An echographic study was undertaken to evaluate left (LV) and right ventricular (RV) function in 30 patients with cystic fibrosis. Echographic recording of the pulmonary and aortic valve echogram permitted measurement of the phases of right and left ventricular systole. The ratio of the LV preejection period/LV ejection time (LPEP/LVET) and shortening of the LV internal dimension %SID was employed to reflect LV function, while RV preejection period/RV ejection time (RPEP/RVET) has excellent correlation with pulmonary artery diastolic pressure. RPEP/RVET and two other echographic measurements, right ventricular wall (RVW) and internal dimension (RVD) were compared with pulmonary function tests and clinical scores. RPEP/RVET correlated well with percent vital capacity(%VC), r = -0.73, percent residual volume (%RVol) r = +0.72, and clinical score, r = -0.77. Multilinear regression of RPEP/RVET, RVD, and RVW improved correlation for %VC (r = -0.80), %RVol, r = +0.82, and clinical score, r = -0.84. Patients in overt right heart failure exhibited elevated RPEP/RVET (mean = 0.48) when compared to patients not in right heart failure (mean = .33). Marked diminution of LV function was present in two patients. A variety of cardiovascular abnormalities were demonstrated echographically and were valuable in assessing the degree of cardiac involvement in patients with cystic fibrosis.

Adolescent↗
PubMed2006

Cholesterol primes vascular smooth muscle to induce Ca2 sensitization mediated by a sphingosylphosphorylcholine-Rho-kinase pathway: possible role for membrane raft.

Hypercholesterolemia is a major risk factor involved in abnormal cardiovascular events. Rho-kinase-mediated Ca(2+) sensitization of vascular smooth muscle (VSM) plays a critical role in vasospasm and hypertension. We recently identified sphingosylphosphorylcholine (SPC) and Src family tyrosine kinase (Src-TK) as upstream mediators for the Rho-kinase-mediated Ca(2+) sensitization. Here we report the strong linkage between cholesterol and the Ca(2+) sensitization of VSM mediated by a novel SPC/Src-TK/Rho-kinase pathway in both humans and rabbits. The extent of the sensitization correlated well with the total cholesterol or low-density lipoprotein cholesterol levels in serum. However, an inverse correlation with the serum level of high-density lipoprotein cholesterol was observed, and a correlation with other cardiovascular risk factors was nil. When cholesterol-lowering therapy was given to patients and rabbits with hypercholesterolemia, the SPC-induced contractions diminished. Depletion of VSM cholesterol by beta-cyclodextrin resulted in a loss of membrane caveolin-1, a marker of cholesterol-enriched lipid raft, and inhibited the SPC-induced Ca(2+) sensitization and translocation of Rho-kinase from cytosol to the cell membrane. Vasocontractions induced by membrane depolarization and by an adrenergic agonist were cholesterol-independent. Our data support the previously unreported concept that cholesterol potentiates the Ca(2+) sensitization of VSM mediated by a SPC/Src-TK/Rho-kinase pathway, and are also compatible with a role for cholesterol-enriched membrane microdomain, a lipid raft. This process may play an important role in the development of abnormal vascular contractions in patients with hypercholesterolemia.

Animals↗
PubMed2003

Serum cardiac troponin and subclinical cardiac status in pediatric chronic renal failure.

BACKGROUND: Patients with uremia often have elevated serum cardiac troponin T (cTnT) even without clinical heart damage. Pediatric patients are ideal for studies of the relationship between uremia and heart disease because they are unlikely to have cardiac risk factors other than uremia. OBJECTIVE: To determine the relationship between uremia and cTnT levels. DESIGN: Echocardiograms and blood chemistry results were obtained from 50 pediatric patients with chronic renal failure and without clinical heart disease. Levels of cTnT were tested for correlation with cardiac dysfunction. In multivariate analysis, biochemical aspects of renal disease and its treatment were tested for correlation with cardiac dysfunction. RESULTS: Forty-nine patients had cardiovascular abnormalities, including increased left ventricular function and mass, elevated heart rate and blood pressure, and reduced LV afterload. LV contractility was inversely correlated with cTnT level (r = -0.36). Higher cTnT also correlated with higher serum creatine kinase-MB mass, lower serum parathyroid hormone, higher blood urea nitrogen and bicarbonate levels, and the use of diuretics, but not with higher cardiac troponin I. Left ventricular contractility was inversely related to serum creatinine, phosphorus, and the use of beta-blockers. CONCLUSIONS: Elevated cTnT levels are not artifactual, but are genuine indicators of cardiomyocyte damage. Cardiac damage, indicated by either elevated cTnT or low LV contractility, is related to uremia, deranged calcium and phosphorus metabolism, and bicarbonate levels. Serum cTnT and LV contractility identify subclinical cardiac damage that could be treated to hopefully reduce cardiovascular morbidity and mortality in this high-risk population.

Adolescent↗
PubMed1998

Clinical and echocardiographic findings in patients with suspected acute aortic dissection.

OBJECTIVES: The objective of this study was to define the range of clinical presentations, echocardiographic findings, and underlying final diagnoses in patients with clinically suspected acute aortic dissection. METHODS AND RESULTS: This study was designed as a retrospective review of clinical and echocardiographic data in consecutive patients evaluated for clinically suspected acute aortic dissection. The study population consisted of 75 studies in 74 consecutive patients referred for urgent or emergency evaluation because of signs and symptoms suggesting acute aortic dissection. A history and physical examination designed to elicit the cause of chest pain, evidence of congestive heart failure, and other cardiovascular abnormalities was performed in each patient. All patients underwent transesophageal echocardiography by experienced operators. Routine 12-lead electrocardiograms and chest radiographs were available for review in the majority of patients. Magnetic resonance imaging or computed tomography was performed in only 5 (6%) and 34 (44%) patients, respectively. Contrast aortography was performed in 21 (27%) patients. For the entire patient cohort, the most prevalent symptom was chest pain alone (n = 31; 41%) or chest pain in conjunction with back pain (n = 23; 31%). Classic "tearing" pain was an infrequent symptom. Syncope or other neurologic findings were present in 15 (20%) patients. Acute aortic dissection was responsible for 34 (45%) of the 75 presentations, with 31 (41% of total evaluations, 92% of dissections) involving the ascending aorta (Stanford type A, DeBakey type 1 or 2). Alternate major cardiovascular diagnoses, including acute myocardial infarction, primary valvular disease, or pericardial disease, were established in 12 (16%) cases. Aortic pathology, other than dissection, was found in 15 (20%) cases. Transesophageal echocardiography established the diagnosis responsible for the symptoms in 61 (81%) cases. CONCLUSIONS: Symptoms in patients with acute aortic dissection are more variable than commonly recognized. Transesophageal echocardiography is an accurate primary diagnostic tool in patients with clinically suspected acute aortic dissection. It allows rapid diagnosis of dissection and can identify alternate cardiovascular pathology responsible for the symptoms in a significant number of patients without acute dissection.

Aged↗
PubMed2003

Prognosis of angina with and without a diagnosis: 11 year follow up in the Whitehall II prospective cohort study.

OBJECTIVE: To investigate the prognosis of angina among people with and without diagnosis by a doctor and an abnormal cardiovascular test result. DESIGN: Prospective cohort study with a median follow up of 11 years. SETTING: 20 civil service departments originally located in London. PARTICIPANTS: 10 308 civil servants aged 35-55 years at baseline. MAIN OUTCOME MEASURES: Recurrent reports of angina; quality of life (SF-36 physical functioning); non-fatal myocardial infarction; death from any cause (n = 344). RESULTS: 1158 (11.4%) participants developed angina, and 813 (70%) had no evidence of diagnosis by a doctor at the time of the initial report. Participants without a diagnosis had an increased risk of impaired physical functioning (age and sex adjusted odds ratio of 2.36 (95% confidence interval 1.91 to 2.90)) compared with those who had neither angina nor myocardial infarction throughout follow up. Among reported cases of angina without a diagnosis, the 15.5% with an abnormality on a study electrocardiogram had an increased risk of death (hazard ratio 2.37 (1.16 to 4.87)). These effects were similar in magnitude to those in participants with a diagnosis of angina. CONCLUSION: Undiagnosed angina was common and had an adverse impact on prognosis comparable to that of diagnosed angina, particularly among people with electrocardiographic abnormalities. Efforts to improve prognosis among people with angina should take account of this submerged clinical iceberg.

Adult↗
PubMed1995

Anti-retinoic acid monoclonal antibody localizes all-trans-retinoic acid in target cells and blocks normal development in early quail embryo.

Avian cardiovascular development is vitamin A-dependent, and retinoic acid has been suggested to be active in this important developmental event. We report here that a monoclonal antibody against all-trans-retinoic acid blocks normal embryonic development in the quail causing cardiovascular abnormalities typical of avian vitamin A deficiency. In whole-mount preparations of stage 5 normal quail embryos the fluorescence associated with the antiretinoic acid monoclonal antibody localizes in Hensen's node and in caudal area. In stage 7-8 embryos fluorescence localizes in heart-forming areas as well as in head mesenchyme, in Hensen's node, in nephrotome, and in caudal area. These studies are the first to localize endogenous all-trans-retinoic acid during very early stages of normal avian development. We propose that all-trans-retinoic acid is biosynthesized in its target cells during early avian embryo-genesis and that the availability of this signal molecule is spatiotemporally regulated. We conclude that all-trans-retinoic acid or a closely related metabolite is the physiological form of vitamin A required for normal cardiovascular development and for other very early developmental events in the quail embryo.

Animals↗
PubMed1989

Should we tell them when their blood pressure is up?

We carried out two studies to determine the effects of feedback on subsequent blood pressure and heart rate readings in subjects without significant cardiovascular abnormalities. In both studies the subjects were randomly assigned to be told that their blood pressure was normal or was high or to receive no feedback at all; 3 minutes later another reading was taken and correct feedback provided. Study 1 was done in 114 patients who attended a family practice teaching unit for an office visit; subjects taking cardioactive medication or with chronically elevated blood pressure (diastolic pressure more than 95 mm Hg) or known low pressure (diastolic pressure less than 60 mm Hg) were excluded. Half of the subjects received feedback from a nurse and the other half from a physician. We found no effect of type of feedback or type of practitioner on subsequent readings. No adaptation of diastolic blood pressure or heart rate took place, whereas a similar rest period in the laboratory consistently triggers cardiovascular adaptation. Given the field nature of the study it was not clear whether the intervention was not powerful or whether the practitioner-patient interactions diffused the effects of an otherwise powerful intervention. Therefore, a second study with the same design was carried out in a controlled laboratory setting with 61 university students who believed they were in the adaptation phase of an experimental stress protocol. The subjects did not interact with the experimenter, who provided only the initial feedback, via intercom. The findings replicated those of study 1: type of feedback had no significant effect on subsequent blood pressure levels, and all types of feedback prevented cardiovascular adaptation. We recommend that patients be allowed to rest alone for at least 10 minutes before blood pressure is measured. Our findings suggest that practitioners need not be concerned about telling normotensive or borderline hypertensive patients that their blood pressure is elevated.

Adult↗
PubMed2005

Cardiovascular changes in mucopolysaccharidoses in Taiwan.

From 1991 to 2002, we managed 72 patients with mucopolysaccharidoses. We retrospectively reviewed the records of 37 for whom detailed physical findings and cardiovascular evaluation were available. Twenty patients had serial electrocardiographic (ECG) examinations, and none had arrhythmias. All 20 patients had low R wave voltage in V6. One type VI patient had ischaemic changes secondary to severe cardiomyopathy at the terminal stage of her disease. Among the 37 patients in whom echocardiography was performed, cardiovascular abnormalities progressed with age, although most had mild clinical signs and symptoms. The most common changes were abnormalities of the mitral and aortic valves hypertrophy of the interventricular septum, especially in types I, II, and VI. During the follow-up period of up to 5 years, 3 type II patients and I type VI patient expired. In at least 3 of these patients, death was related to cardiopulmonary failure. As MPS patients are surviving longer, complete cardiac evaluation at regular intervals is mandatory and should be part of their routine assessment.

Age Distribution↗
PubMed2003

The value of autopsy in pediatric cardiology and cardiovascular surgery.

Autopsy has been considered extremely helpful in determining the accuracy of the premorbid diagnosis. With recent advances in diagnostic imaging, the value of the autopsy has been called into question. The aim of this study was to assess the value of the pediatric autopsy in the current era of advanced diagnostic technology and sophisticated surgical intervention for congenital heart disease (CHD) and also to determine the autopsy's potential impact on clinical management. We compared the data from the postmortem examination of 29 children with CHD with the data obtained before death and evaluated for the accuracy of the diagnosis of the cardiac anatomy as well as the cause of death. The diagnosis of the anatomy was confirmed in 13 cases (45%), additional cardiovascular abnormalities with potential clinical impact were found in 11 cases (38%), and additional abnormalities without clinical impact were found in 5 cases (17%). The cause of death was confirmed in 15 cases (52%), determined by autopsy in 12 cases (41%), and uncertain in 2 cases (7%). We conclude that the pediatric autopsy continues to provide clinically relevant information with a potential impact on patient management and to reveal unexpected causes of death in a significant proportion of patients with CHD.

Adolescent↗
PubMed2005

Syphilitic coronary artery ostial stenosis resulting in acute myocardial infarction and death.

Cardiovascular abnormalities are well-known manifestations of tertiary syphilis infections. Most notable in this regard is syphilitic aortitis, which tends to result in aortic root dilatation and its associated complications. A less common manifestation of syphilitic aortitis is coronary artery ostial narrowing related to aortic wall thickening. Herein, we present the case of a 32-year-old female who died of a myocardial infarct due to coronary artery ostial stenosis secondary to syphilitic aortitis.

Adult↗
PubMed2006

Model systems for the study of heart development and disease. Cardiac neural crest and conotruncal malformations.

Neural crest cells are multipotential cells that delaminate from the dorsal neural tube and migrate widely throughout the body. A subregion of the cranial neural crest originating between the otocyst and somite 3 has been called "cardiac neural crest" because of the importance of these cells in heart development. Much of what we know about the contribution and function of the cardiac neural crest in cardiovascular development has been learned in the chick embryo using quail-chick chimeras to study neural crest migration and derivatives as well as using ablation of premigratory neural crest cells to study their function. These studies show that cardiac neural crest cells are absolutely required to form the aorticopulmonary septum dividing the cardiac arterial pole into systemic and pulmonary circulations. They support the normal development and patterning of derivatives of the caudal pharyngeal arches and pouches, including the great arteries and the thymus, thyroid and parathyroids. Recently, cardiac neural crest cells have been shown to modulate signaling in the pharynx during the lengthening of the outflow tract by the secondary heart field. Most of the genes associated with cardiac neural crest function have been identified using mouse models. These studies show that the neural crest cells may not be the direct cause of abnormal cardiovascular development but they are a major component in the complex tissue interactions in the caudal pharynx and outflow tract. Since, cardiac neural crest cells span from the caudal pharynx into the outflow tract, they are especially susceptible to any perturbation in or by other cells in these regions. Thus, understanding congenital cardiac outflow malformations in human sequences of malformations as represented by the DiGeorge syndrome will necessarily require understanding development of the cardiac neural crest.

Animals↗
PubMed1995

The varied manifestation of pulmonary artery agenesis in adulthood.

OBJECTIVE: Unilateral pulmonary artery agenesis (UPAA), a rare congenital anomaly that is frequently associated with other cardiovascular abnormalities, is usually diagnosed in childhood. Most patients who have no associated cardiac anomalies have only minor or absent symptoms and survive into adulthood. The conditions of such patients are frequently misdiagnosed in adulthood. In this report, we describe six patients with UPAA in whom the diagnosis was first established in adulthood. The varied clinical presentation of these patients is reviewed and the relative effectiveness of a variety of diagnostic tests is compared. SUBJECTS AND METHODS: During the period January 1987 through December 1990, six male patients, aged 17 to 20 years, were found to have UPAA at the time of their medical screening for enrollment into the armed forces. The diagnosis was based on history, clinical and imaging examinations, including chest radiography, ventilation-perfusion lung scan, digital subtraction angiography (DSA), computed tomography (CT), and magnetic resonance imaging (MRI). RESULTS: In four of the patients, the UPAA was on the left side and in two it was on the right. A right aortic arch was present in three patients and other cardiovascular anomalies were found in three. Pulmonary function studies showed a mild restrictive pattern in four. In contrast to previous reports, the ventilation scan showed a diminished "wash in" and "equilibrium" phase without a delayed "wash out" phase on the affected side in all patients. Selective bronchography through the fiberoptic bronchoscope revealed ipsilateral mixed-type bronchiectasis in two of four patients studied, a finding of clinical significance that has not been described previously. In all cases, the diagnosis was made by DSA. CT of the thorax (n = 6) and MRI (n = 4) were diagnostic in all cases in which they were performed, but added no significant information. CONCLUSION: UPAA is frequently misdiagnosed in adulthood and is often not considered in the differential diagnosis of the unilateral hyperlucent lung. Clinicians and radiologists should be aware of the possibility of undiagnosed cases in adults, with many atypical characteristics.

Adolescent↗
PubMed2005

Cardiomyopathy associated with microcirculation dysfunction in laminin alpha4 chain-deficient mice.

Laminin alpha4 chain is a component of extracellular matrix (ECM) laminin-8 and -9 and serves dual roles as a structure protein and as a signaling molecule. The abundance of laminin alpha4 chain transcripts in the heart suggests an important role of this protein in cardiovascular development and function. In this study, we demonstrate that laminin alpha4 deficient mice gradually develop cardiac hypertrophy with impaired function. We show that depletion of laminin alpha4 chain did not alter the levels of dystrophin-glycoprotein complex (DGC) components or affect cell membrane integrity. No alteration in integrin beta 1D protein was observed in terms of expression level or distribution pattern, indicating that the postnatal development of cardiac hypertrophy and cardiomyopathy in these mice is unlikely associated with the stability of sarcolemmal DGC and integrin complexes. Moreover, cardiomyocytes isolated from Lama4-/- mutant hearts maintained their contractility in vitro. In contrast, elevated levels of hypoxia-inducible factor 1alpha (Hif1alpha) and vascular endothelial growth factor A (Vegfa) transcripts, along with multiple foci of cardiomyocyte degeneration and fibrosis suggested sustained cardiac ischemia. Electron microscopy confirmed malformed blood vessels and wide pericapillary ECM spaces, suggesting the presence of microcirculation abnormalities in Lama4-/- mutant hearts. We thus conclude that mutation in the laminin alpha4 chain leads to abnormal cardiovascular ECM structure that cause insufficient oxygen supply to the heart and the subsequent ischemic cardiac phenotype observed. Our study links the genetic deficiency of an ECM protein to cardiomyopathy and implies a novel pathway of idiopathic cardiomyopathy in human.

Animals↗
PubMed1990

Pseudomonas aeruginosa compared with Escherichia coli produces less endotoxemia but more cardiovascular dysfunction and mortality in a canine model of septic shock.

We investigated the effects of two different Gram-negative bacteria and radiation-induced leukopenia on endotoxemia, cardiovascular abnormalities, and mortality in a canine model of septic shock. Serial hemodynamics were measured in conscious dogs using radionuclide heart scans and thermodilution cardiac output catheters. Plasma endotoxin concentrations were determined with a chromogenic Limulus amebocyte lysate assay. Viable Pseudomonas aeruginosa or Escherichia coli implanted intraperitoneally produced concordant hemodynamic patterns of septic shock (p less than 0.01). Endotoxin concentrations were more than tenfold lower in dogs infected with P aeruginosa compared with E coli (p less than 0.0001). Despite lower endotoxin levels, P aeruginosa-infected dogs had a higher mortality (p less than 0.01), more severe hypotension (p less than 0.05), and greater depression of the left ventricular ejection fraction (p less than 0.05) than dogs with E coli sepsis. A nonlethal E coli challenge combined with leukopenia (induced by a nonlethal dose of radiation) resulted in a mortality of 60 percent (p less than 0.01) without greater cardiovascular dysfunction or higher endotoxin concentrations. These findings suggest that bacterial products other than endotoxin and host-related factors may be important contributors to the toxicity, cardiovascular instability, and mortality of Gram-negative septic shock. Quantitative determinations of plasma endotoxin are unlikely to correlate with the clinical severity of septicemia in heterogeneous patient populations infected with different Gram-negative organisms.

Animals↗
PubMed1995

[Relationship between blood pressure determination anxiety and hypertensive complications].

To assess the clinical significance of the reaction to blood pressure measurement, 1,013 (889 men) borderline to severe hypertensive patients, enrolled between 1984 and 1993, were studied. Their mean age (+/- SE) was 33.6 +/- 0.46 (range 16-75 years) and their mean office blood pressure (+/- SE) was 152.3 +/- 0.56/95.5 +/- 0.39 mmHg. All subjects underwent ambulatory blood pressure monitoring, ECG and fundoscopy. On the basis of the latter two tests a target organ damage score was calculated, from 0 (no abnormalities) to 5 (maximum severity). In 731 patients an echocardiogram was also performed. The white-coat effect was assessed by measuring the regression of office blood pressure on ambulatory blood pressure and calculating the residual office blood pressure. The subjects with high residual blood pressure showed a greater degree of age-adjusted target organ damage compared to those with intermediate or low residual blood pressure (systolic p < 0.0001; diastolic p = 0.04). Age-adjusted left ventricular mass was influenced by residual diastolic blood pressure (p < 0.0001). In a stepwise multiple regression analysis, where age, ambulatory blood pressure levels, sex and duration of hypertension were added to the model, residual blood pressure showed a relationship with the degree of target organ damage and left ventricular mass. In conclusion, the present results show that the white-coat-effect is not innocent, as it is associated with a high degree of cardiovascular abnormalities.

Adolescent↗
PubMed2004

Autonomic dysregulation as a basis of cardiovascular, endocrine, and inflammatory disturbances associated with obstructive sleep apnea and other conditions of chronic hypoxia, hypercapnia, and acidosis.

Obstructive sleep apnea has traditionally been viewed as a structural disease. A multitude of systemic endocrine and cardiovascular abnormalities have been previously attributed to the prevalence of obesity in these patients. A growing body of clinical evidence, however, points to a relationship between sleep apnea and its systemic abnormalities independent of obesity. We hypothesize that this association is based on a maladaptive autonomic response of chemoreceptors, reacting to the hypoxia, hypercapnia, and acidosis of sleep apnea. The elevated sympathetic response triggers an inflammatory cascade that results in a myriad of downstream consequences including insulin resistance, hypertension, diabetes, atherosclerosis and metabolic syndrome. The sympathetic bias and endocrine disturbances may further exacerbate sleep disturbance in a potentially pernicious cycle. Our proposal may extend to any chronic respiratory or metabolic conditions that manifest hypoxia, hypercapnia, and acidosis and elicit a maladaptive autonomic and inflammatory response.

Acidosis↗
PubMed2006

Oxidative stress, inflammation and early cardiovascular damage in children with chronic renal failure.

The relationship between inflammation, oxidant stress and cardiovascular damage in children with chronic renal failure (CRF) has not previously been investigated. The aim of this study was to investigate markers of oxidative stress, inflammation and early cardiovascular abnormalities. Therefore, erythrocyte superoxide dismutase (SOD) and catalase (CAT) activities; blood glutathione (GSH) and serum malondialdehyde (MDA) levels; C-reactive protein (CRP) and proinflammatory cytokines (IL-6, TNF-alpha,); and left ventricular masses (LVM) and intima media thicknesses (IMT) were measured in children with CRF. A total of 29 children with CRF (19 nondialysis, 10 peritoneal dialysis) were included. The control group consisted of 25 healthy subjects. CRF children had significantly increased IL-6, TNF-alpha, CRP and MDA concentrations and decreased SOD, CAT and GSH levels compared with controls (P<0.05). Nondialysis and peritoneal dialysis subgroups had similar oxidative stress and inflammation biomarkers (P>0.05). Erythrocyte CAT was positively correlated with CRP, TNF-alpha, and IL2-R in the study group. Positive correlations were found between cytokine concentrations, CRP and urea/creatinine levels. Significantly increased LVM and IMT values were found in CRF children (P<0.05). In conclusion, increased oxidant stress and inflammation together with early cardiovascular damage were found in CRF children. Further studies with more patients are needed to verify these results.

Cardiovascular Diseases↗
PubMed1998

Interictal cardiovascular autonomic responses in patients with epilepsy.

PURPOSE: To evaluate the interictal autonomic nervous system function in 84 patients with epilepsy: 37 with newly diagnosed, previously untreated epilepsy, and 47 patients receiving long-term carbamazepine (CBZ), phenytoin (PHT), or valproate (VPA) monotherapy, or CBZ plus PHT, or CBZ plus VPA for their seizure disorder. METHODS: We assessed autonomic control of the cardiovascular regulatory system by standardized cardiovascular reflex tests measuring changes in heart rate (HR) and blood pressure (BP) at rest and after certain stimuli. RESULTS: The HR and BP responses were similar to those of control subjects in patients with newly diagnosed epilepsy. However, HR variation during normal breathing and maximum systolic BP increase in isometric work were diminished in patients, who had been treated with antiepileptic drugs (AEDs) for epilepsy for a long time. Diminished HR responses to the Valsalva maneuver were noted in patients receiving CBZ as monotherapy and during deep breathing in patients receiving CBZ combined with PHT or VPA. Furthermore, patients receiving CBZ had diminished BP responses in isometric work. When analyzed in relation to epilepsy type, suppressed HR responses in normal breathing were associated with primary generalized epilepsy (PGE), whereas diminished BP responses in isometric work were associated with partial epilepsy. Two patients with recently diagnosed partial epilepsy and 1 patient receiving long-term CBZ monotherapy for partial epilepsy had two abnormal cardiovascular response test results. CONCLUSIONS: Our results show that cardiovascular responses mediated by both the parasympathetic and sympathetic nervous system are diminished in patients with epilepsy. However, the changes appear to be clinically significant in only a few of them and appear to be associated with CBZ medication. Further studies are needed to detect the underlying complex interactions and clinical significance of autonomic nervous system dysfunction in patients with epilepsy.

Adolescent↗