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PubMed2005

Selective management of cardiovascular dysfunction in posttraumatic SIRS and sepsis.

Cardiovascular dysfunction associated with the systemic inflammatory response syndrome (SIRS) is caused by a combination of decreased myocardial contractility and low vascular resistance. The contribution of each of these components can be determined at the bedside, and directed therapy can be appropriately initiated. Over an 8-month period of time, 23 consecutive patients who experienced posttraumatic SIRS while still being monitored with a volumetric pulmonary artery catheter (PAC) were prospectively evaluated. Ventricular pressure-volume diagrams were constructed to quantify myocardial contractility and afterload. In a resuscitation protocol, dobutamine was administered to patients with an isolated decrease in contractility, and dopamine or epinephrine was instituted for the combination of reduced contractility and afterload. Variables describing cardiovascular function were measured at the time of resolution of initial shock resuscitation (BASE), at the onset of SIRS (ONSET), and after administration of inotropic or vasoactive agents (TREAT). ONSET was associated with a significant decrease in left ventricular power (LVP) (362 +/- 96 to 235 +/- 55 mmHg.L/min/m(2), P < 0.00001) and stroke work index (SWI) (4670 +/- 1213 to 3060 +/- 848 mmHg.mL/m, P < 0.00001) from BASE. Sixteen patients (70%) demonstrated predominantly decreased contractility, which returned to near BASE values after the administration of dobutamine. The remaining seven patients (30%) had both decreased contractility and afterload, which was treated with dopamine or epinephrine. LVP and SWI significantly increased (235 +/- 55 to 328 +/- 77 mmHg.L/min/m(2), P < 0.00001, and 3060 +/- 848 to 4554 +/- 1423 mmHg.mL/m(2), P < 0.00001, respectively) on the initiation of directed therapy. Specific cardiovascular abnormalities can be identified at the bedside, and this information can guide pharmacologic management. Directed therapy improves cardiovascular function.

Adult↗
PubMed1976

Dynamic pituitary testing in a female with Kallman's syndrome and associated cardiac anomaly.

A patient with Kallman's syndrome and an anomalous right aortic arch is described. Dynamic pituitary testing was carried out revealing no significant response of prolactin to chlorpromazine stimulation or water loading suppression. A normal response of growth hormone to insulin induced hypoglycemia was observed. These data are interpreted as indicating a primary hypothalamic abnormality in Kallman's syndrome. In addition, this is the first report of the association of a cardiovascular abnormality with Kallman's syndrome.

Adolescent↗
PubMed1999

Role of cardiac structural and functional abnormalities in the pathogenesis of hyperdynamic circulation and renal sodium retention in cirrhosis.

The aim of this study was to assess the relationship between subtle cardiovascular abnormalities and abnormal sodium handling in cirrhosis. A total of 35 biopsy-proven patients with cirrhosis with or without ascites and 14 age-matched controls underwent two-dimensional echocardiography and radionuclide angiography for assessment of cardiac volumes, structural changes and systolic and diastolic functions under strict metabolic conditions of a sodium intake of 22 mmol/day. Cardiac output, systemic vascular resistance and pressure/volume relationship (an index of cardiac contractility) were calculated. Eight controls and 14 patients with non-ascitic cirrhosis underwent repeat volume measurements and the pressure/volume relationship was re-evaluated after consuming a diet containing 200 mmol of sodium/day for 7 days. Ascitic cirrhotic patients had significant reductions in (i) cardiac pre-load (end diastolic volume 106+/-9 ml; P<0.05 compared with controls), due to relatively thicker left ventricular wall and septum (P<0.05); (ii) afterload (systemic vascular resistance 992+/-84 dyn.s.cm(-5); P<0. 05 compared with controls) due to systemic arterial vasodilatation; and (iii) reversal of the pressure/volume relationship, indicating contractility dysfunction. Increased cardiac output (6.12+/-0.45 litres/min; P<0.05 compared with controls) was due to a significantly increased heart rate. Pre-ascitic cirrhotic patients had contractile dysfunction, which was accentuated when challenged with a dietary sodium load, associated with renal sodium retention (urinary sodium excretion 162+/-12 mmol/day, compared with 197+/-12 mmol/day in controls; P<0.05). Cardiac output was maintained, since the pre-load was normal or increased, despite a mild degree of ventricular thickening, indicating some diastolic dysfunction. We conclude that: (i) contractile dysfunction is present in cirrhosis and is aggravated by a sodium load; (ii) an increased pre-load in the pre-ascitic patients compensates for the cardiac dysfunction; and (iii) in ascitic patients, a reduced afterload, manifested as systemic arterial vasodilatation, compensates for a reduced pre-load and contractile dysfunction. Cirrhotic cardiomyopathy may well play a pathogenic role in the complications of cirrhosis.

Adult↗
PubMed1984

Lithium adverse reactions in psychiatric patients.

A brief review of the literature on the adverse reaction of lithium therapy in man is presented. This was aimed at both toxic and side effects of lithium on various organ systems of the body. Inconclusive, insufficient or conflicting data were found in several areas of possible lithium-induced toxicity, notably in lithium-associated nephrotoxicity. Results of prospective studies are needed to clarify this issue. Adverse reactions derived from continued administration of lithium salts with neuroleptic medications or with electroconvulsive therapy were also reviewed. Lithium-induced side effects on the endocrine and gastrointestinal systems were also summarized along with both dermatologic and ophthalmologic effects. The teratogenicity of lithium during pregnancy and its cardiovascular abnormalities were discussed. The target organs of lithium poisoning and their management were also presented.

Abnormalities, Drug-Induced↗
PubMed2004

Phytosterols decrease prostaglandin release in cultured P388D1/MAB macrophages.

Cardiovascular disease (CVD) remains the leading cause of death in Western societies. Atherosclerosis is a major cardiovascular related disorder that is responsible for 50% of all mortality in the United States. Several epidemiological studies suggest that consumption of a plant-based diet is associated with a decreased incidence of cardiovascular abnormalities. Phytosterols, especially beta-sitosterol, are plant sterols that have been shown to exert protective effects against cardiovascular diseases as well as many types of cancer. Monocyte/macrophage cells are involved with the inflammatory process. Accumulation of these cells in arteries is one of the initial events leading to atherosclerosis. Macrophages are capable of supplying the atherosclerotic vessel with substantial amounts of prostaglandins. Prostaglandins have been shown by numerous studies to play a key role in the atherosclerosis process. They can affect platelet aggregation, vasodilation or constriction of blood vessels, and the adherence of monocytes to the vessel walls. The purpose of this study was to examine the effect of phytosterols on the release of PGE(2) and PGI(2) from lipopolysaccharide (LPS)-stimulated P388D(1)/MAB macrophage cells. P388D(1)/MAB cells were supplemented with 16 microM cholesterol, beta-sitosterol or campesterol using cyclodextrin as a vehicle. Phytosterol supplementation led to a significant decrease in cellular growth at various time points throughout a 7-day treatment period, especially after 3 days of treatment. Macrophages incorporated the supplemented phytosterols into their membranes which accounted for 26% of total membrane sterols. Cholesterol supplementation at 16 microM however, had no effect on membrane sterols. Supplementation with 16 microM concentration of beta-sitosterol or campesterol resulted in a significant inhibition of PGE(2) and PGI(2) release from macrophage cells as compared to the vehicle control. Of the two phytosterols, beta-sitosterol supplementation exhibited a greater inhibitory effect. PGE(2) release was decreased 68% by beta-sitosterol and 55% by campesterol, while cholesterol supplementation was not as effective, as it led to a 37% decrease. Similarly, release of PGI(2) from macrophages was inhibited 67% by beta-sitosterol and 52% by campesterol treatment, while enrichment of the cells with cholesterol, led to a 35% decrease in PGI(2) release. The decrease in prostaglandin release was not due to alteration in the expression of cPLA(2) and COX-2 enzymes which suggests that alterations in the activities of these enzymes may be responsible for the observed changes in prostaglandin release. It was concluded that phytosterol incorporation into macrophages may offer protection from atherosclerosis by reducing their prostaglandin release and thus slowing down the atheroma development.

Animals↗
PubMed2001

Physician-performed point-of-care echocardiography using a laptop platform compared with physical examination in the cardiovascular patient.

OBJECTIVES: The purpose of this study was to compare the results of physical examinations (PEs) performed by board-certified cardiologists with the results of point-of-care (POC) echocardiography in a group of patients with cardiovascular disease. BACKGROUND: Although cardiovascular PE is crucial in the evaluation of patients with suspected heart disease, the skills required to diagnose abnormal cardiovascular findings have been declining. Echocardiography is a powerful noninvasive cardiovascular diagnostic tool; however, echocardiographic evaluation of patients is not performed at the time of patient encounter (POC echocardiography), beacuse current platforms are cumbersome and expensive for individual physician use. The development of miniaturized echocardiographic equipment has the potential to overcome some of these limitations. METHODS: Thirty-six subjects had a complete cardiovascular examination by four board-certified cardiologists. The physicians subsequently imaged each patient using a miniaturized echocardiographic platform. The yield of PE and POC echocardiography were compared using a complete echocardiographic study as the gold standard, performed on an upper-end platform. RESULTS: Cardiac examination failed to detect 59% of the overall cardiovascular findings. Physician-performed echocardiography with the prototype device missed 29% of the overall cardiovascular pathology. When considering only the major cardiovascular findings, the cardiologists' PEs still failed to correctly detect 43%. Point-of-care echocardiography reduced this to 21% without significant interphysician variation. CONCLUSIONS: Point-of-care echocardiography using a miniaturized echocardiographic platform substantially improved the detection of important cardiovascular pathology compared with PE. Use of this device by a cardiovascular specialist with training in echocardiography as a routine adjunct to PE appears to be useful.

Echocardiography↗
PubMed2003

Evidence of cardiac ischemia during seizures in drug refractory epilepsy patients.

The authors investigated whether patients with drug refractory epilepsy have cardiovascular abnormalities that might be related to a high frequency of sudden death. Twenty-three subjects underwent comprehensive cardiovascular evaluations before and during video-EEG monitoring. ST-segment depression occurred in 40% and was associated with a higher maximum heart rate during seizures. These data suggest that cardiac ischemia may occur in these patients.

Adult↗
PubMedDate not supplied

[Leber's hereditary optic neuropathy].

233 personal cases of leber's optic neuropathy have been analyzed by the authors in order to present clinical symptoms, evolution and genetic aspects. A group of 23 patients, in which 7 presented the disease and the others were asymptomatic members of families with the disease, was analyzed on evaluation of abnormalities of evoked visual responses; An other similar group, in repartition of subjects, was analyzed on frequency of cardiovascular abnormalities. The results have been analyzed and discussed about the role of predictive symptoms in diagnosis of the acute phase of the disease.

Adolescent↗
PubMed1997

The aquatic vertebrate embryo as a sentinel for toxins: zebrafish embryo dechorionation and perivitelline space microinjection.

Pollution of aquatic ecosystems poses a serious threat to aquatic organisms and ultimately the entire ecosystem. Understanding how a toxin affects embryonic development is key to determining the risk a pollutant represents to the environment. Extraembryonic membranes, such as the chorion of fish eggs, provide a protective barrier between the embryo and the environment. Although the fish chorion excludes many chemical pollutants, some noxious agents can still gain access to the aquatic embryo. Therefore a monitoring system that tests the effects directly upon the embryo must be established. Although exposure to a single toxin in the laboratory can determine the concentration at which a pollutant becomes a health or environmental hazard, embryos and adults in nature are not merely affected by a single chemical, but are exposed to mixtures of different pollutants. Zebrafish (Danio rerio) and medaka (Oryzias latipes) embryos were employed for the rapid observation of the effects of single chemicals and chemical mixtures on development. Using dechorionation and a perivitelline space microinjection system, the embryos were effective sentinels for low concentrations of aquatic pollutants. The developmental effects of small quantities of toxins were observed. Embryos treated during the late gastrula stage of development with hexachlorobenzene (HCB); 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); toluene; benzene; or mixtures of these chemicals developed cardiovascular abnormalities. The zebrafish dechorionation exposure technique, Micro Intrachorionic Zebrafish Embryo Live Laboratory test, was especially effective in testing the pollutant mixtures. Combinations of both TCDD and benzene (as well as the toluene and benzene combinations) were tested and the mixtures acted synergistically; the combinations were more toxic than either chemical by itself. Hexachlorobenzene- and TCDD-treated embryos tested positively for expression of cytochrome P450 1A indicating that the cytochrome metabolic pathways were already functional in these early embryos, and suggested that a product of the cytochrome system may be involved in HCB and TCDD pollution associated cardiovascular defects.

Abnormalities, Drug-Induced↗
PubMed1996

Clinical models of cardiovascular regulation after weightlessness.

After several days in microgravity, return to earth is attended by alterations in cardiovascular function. The mechanisms underlying these effects are inadequately understood. Three clinical disorders of autonomic function represent possible models of this abnormal cardiovascular function after spaceflight. They are pure autonomic failure, baroreflex failure, and orthostatic intolerance. In pure autonomic failure, virtually complete loss of sympathetic and parasympathetic function occurs along with profound and immediate orthostatic hypotension. In baroreflex failure, various degrees of debuffering of blood pressure occur. In acute and complete baroreflex failure, there is usually severe hypertension and tachycardia, while with less complete and more chronic baroreflex impairment, orthostatic abnormalities may be more apparent. In orthostatic intolerance, blood pressure fall is minor, but orthostatic symptoms are prominent and tachycardia frequently occurs. Only careful autonomic studies of human subjects in the microgravity environment will permit us to determine which of these models most closely reflects the pathophysiology brought on by a period of time in the microgravity environment.

Autonomic Nervous System↗
PubMed2002

Infants with single ventricle: a population-based epidemiological study.

BACKGROUND: Single ventricle, a rare congenital cardiac defect, often occurs as part of a complex group of cardiovascular abnormalities. Little is known of its epidemiologic associations. METHODS: Using data from the Baltimore-Washington Infant Study [BWIS], (1981-89), a population based case-control study of cardiovascular malformations, infants with single ventricle were evaluated with respect to infant and family characteristics and maternal and paternal exposures. The cases were analyzed according to presence/absence of abnormal cardio-visceral situs. Controls were 3,572 infants without heart defects randomly selected from the regional cohort of live births. Odds ratios and 95% confidence intervals were used as measures of association. RESULTS: Single ventricle occurred in 1.25% of infants with congenital cardiovascular defects in the BWIS. Fifty-five infants had single ventricle. In 48 families (87.3%) the parents were interviewed. Thirty-three infants had normal situs and 15 had abnormal situs. Paternal alcohol consumption (OR = 2.0, 95% CI 1.1-3.9) and paternal cigarette smoking (OR = 2.4, 95% CI 1.1-5.1) were associated with all cases of single ventricle. These associations were even stronger in the subset of infants with abnormal situs. Maternal history of a previous induced abortion was also associated with infants born with abnormal situs (OR = 3.2, 95% CI 1.1-11.5). Paternal marijuana use was associated with cases of single ventricle in normal situs (OR = 2.2, 95% CI 1.0-5.2). CONCLUSIONS: Potential risk factors included paternal smoking and alcohol consumption, highlighting the need for future studies to consider environmental factors in the pathogenesis of this cardiac defect.

Adult↗
PubMed2004

Mechanisms of cardiovascular dysregulation during alcohol withdrawal.

Alcohol withdrawal (AW) is often accompanied by functional cardiovascular abnormalities which return to normal in few days. However, in some patients, they can predict future alterations in the cardiovascular system, even if they remain in abstinence. These changes are mediated by several central and peripheral mechanisms closely related to AW. The level of activation in the sympathetic nervous system is an important factor regulating the functioning of the cardiovascular system in AW directly and/or indirectly with L-type calcium channels and nitric oxide (NO). Other factors may contribute to cardiovascular alterations in AW including the renin-angiotensin-aldosterone system, vasopressin, cortisol and sodium sensitivity. Monitoring of the cardiovascular system is needed in patients undergoing treatment for AW. The patients with elevated systolic blood pressure (SBP) and diastolic blood pressure (DBP) after resolution of AW may require a fuller work-up of their cardiovascular system.

Alcohol-Induced Disorders↗