Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty patients (26 men, 4 women) aged from 32 to 73 years (mean 54 years) who developed anterior (14 cases) or posterior (16 cases) myocardial infarction received intravenous streptokinase in doses of 1,500,000 units 2 to 10 hours (mean 4 hours) after the onset of infarction. Coronary angiography, performed 18.6 days on average after thrombolysis, showed a distinct predominance of asymmetrical stenosis with irregular walls and a narrow neck (10 cases, 33 p. 100) or of complete occlusion (12 cases, 40 p. 100) in the artery responsible for the infarction. Complete occlusion probably was the ultimate stage of stenosis. In contrast, the various angiographic images observed in arteries unrelated to the infarction were evenly distributed. The radiological morphology of coronary arterial lesions after a recent infarction is suggestive of ruptured atheromatous plaque, sometimes complicated by thrombosis in situ. Identical images are seen in unstable angina. These findings indicate that one single therapeutic approach should be applied to the most severe types of coronary disease due to atherosclerosis.
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PMID:[Angiographic morphology of the coronary arteries after a recent myocardial infarction treated by intravenous thrombolysis]. 249 70

Following myocardial infarction, there are structural changes in the surviving restmyocardium, including excentric hypertrophy. These changes are called "remodelling". It includes hypertrophy of the terminally differentiated cardiocytes and proliferation of other myocardial cells (e.g. connective tissue). In the hypertrophied cardiocytes, the pattern of gene expression is changing towards a perinatal-like phenotype. This phenotype change is called "dedifferentiation" and includes (among others) several critical alterations in myocyte Ca+(+)-homeostasis and electromechanical coupling: prolongation of the action potential and thereby augmented Ca+(+)-inflow into the cardiocyte during activation; reduced expression of sarcoplasmic reticulum Ca+(+)-ATPhase with retarded endsystolic Ca+(+)-reaccumulation into the sarcoplasmic reticulum; enhanced expression of the sarcolemmal Na(+)-Ca+(+)-exchanger with enhanced Ca+(+)-export via this rheogenic, asymmetrical exchanger, this export associated with depolarizing netto-inward current. Due to this phenotype constellation, high heart rates can induce cytosolic Ca+(+)-overload, relaxation abnormalities, depressed systolic force-frequency relations, and diastolic Ca+(+)-induced Ca+(+)-release leading to late afterdepolarizations and triggering ventricular tachyarrhythmias. While the poorly differentiated cardiocytes of newborns have a phenotype similar to that in hypertrophied dedifferentiated cardiocytes of overloaded myocardium (at least in some aspects of Ca+(+)-homeostasis), the neonatal heart is protected against arrhythmias by its high intercellular coupling (high density of "gap-junctions") and by its lower size. In contrast, the intercellular coupling in overloaded myocardium is often heterogeneous, the density of gap junctions is globally reduced, and the conductance of gap-junctions is functionally reduced by cytosolic Ca+(+)-overload. This enhances the susceptibility for arrhythmias due to "reentry" as well as due to focal depolarization of multiple origins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Myocardial hypertrophy after myocardial infarct: what is the significance of phenotype changes in cardiocytes?]. 812 18

Four cases of adrenal insufficiency due to bilateral adrenal haemorrhage in patients with antiphospholipid syndrome are reported. The 1st patient had repeated episodes of thrombosis on a background of altered general condition; he was examined by computed tomography (CT) which showed enlarged and presumably tumoral adrenal glands; adrenal insufficiency was present and improved under hormone replacement therapy; the thrombotic episodes were attributed to the antiphospholipid antibodies; after a 5-year follow-up the antiphospholipid syndrome remained alone, and further examinations showed progressive adrenal atrophy. The 2nd patient had systemic lupus erythematosus with thrombocytopenia; because of abdominal pain CT was performed, showing bilateral adrenal enlargement; treatment with intravenous pulses of cyclophosphamide and high-dose immunoglobulins combined with corticosteroids failed, and splenectomy was performed disclosing an old adrenal haematoma which was evacuated. The 3rd patient had bilateral and asymmetrical adrenal hypertrophy at CT; subsequently, systemic lupus erythematosus was diagnosed with anti-prothrombinase and anticardiolipin accounting for the initial findings; follow-up examinations showed the formation of pseudocysts in the adrenals; following myocardial infarction the patient died of cerebral haemorrhage, and autopsy confirmed the presence of old, bilateral adrenal haematomas. The 4th patient had recurrent vein thrombosis associated with distal ischaemia, which prompted CT in search of a neoplasia; this examination revealed 2 large adrenal haematomas while anticardiolipin antibodies were found. In patients with antiphospholipid syndrome any functional or morphological abnormality of the adrenals should prompt a search for bilateral adrenal haemorrhage. Conversely, in all cases of adrenal insufficiency a search for antiphospholipid antibodies should be part of all aetiological investigations, and this search should be carried out prior to withdrawing corticosteroids in cases of systemic lupus erythematosus with antiphospholipid antibodies.
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PMID:[Antiphospholipid syndrome. A new cause of bilateral hemorrhage of the adrenal glands. 4 cases]. 851 Nov 42

Early repolarization (ER) is an enigma. The purpose of this review is to reemphasize the overall electrocardiographic (ECG) pattern of this normal ST variant which continues to challenge the clinician because of its similarity to the current of injury potential to myocardium or an acute pericarditis. The data were provided from the studies identified through computerized searches of Medline, Toxline, Oxford, Agricola, and Bios Afterdark, Cumulative index, and a review of bibliographies of relevant articles on the related subjects. Early repolarization has elevated, upward, concave ST segments, located commonly in precordial leads, with reciprocal depression in a VR, tall, peaked and slightly asymmetrical T waves with notch, and slur on the R wave. The other accompanying features in the ECG are vertical axis, shorter and depressed P-R interval, abrupt transition, counterclockwise rotation, presence of U waves, and sinus bradycardia. Males dominate and patients are often younger than 50 years of age. The incidence of 1 to 2% is found equally common in all races. Degree and incidence of ST elevation decrease as age advances. Exercise or isoproterenol administration may normalize the ST segment. Early repolarization is a benign condition. If the ECG conforms to a classical pattern of ER on serial ECGs, it would exclude the unnecessary hazards of present day revascularization therapy for myocardial infarction such as primary angioplasty or thrombolytic therapy, or aggressive management of acute pericarditis, and so forth. This review concludes with a discussion of comparative ECG features of ER, pericarditis, and myocardial infarction, and provides an algorithm for diagnostic management of patients suffering from these conditions.
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PMID:Early repolarization. 1006 41

Congestive heart failure(CHF) is usually associated with impaired left ventricular(LV) systolic function, and thus, the measurement of systolic function is an essential component of the evaluation of any patients with known or suspected cardiac disease. Among many parameters, most frequently used are LV percent fractional shortening and ejection fraction(EF), which can be easily measured from an M-mode echocardiogram. However, these M-mode measurements may be inaccurate in patients with asymmetrical LV due to myocardial infarction, right ventricular overload or sigmoid septum. Especially in such cases, EF should be measured using two-dimensional echocardiography. Usually, LV volumes and EF are calculated using the disc-summation method through the manual tracing of apical two-chamber and four-chamber echocardiograms. On the other hand, it has been recognized that congestive heart failure may arise in the absence of any systolic dysfunction and CHF due to systolic dysfunction never occurs in the absence of concomitant diastolic dysfunction. Although the analysis of pulsed-Doppler transmitral flow velocity has been most widely used for the noninvasive assessment of LV diastolic function, an increase in left atrial pressure during CHF can pseudonormalize an abnormal flow pattern and mask LV diastolic dysfunction. Recently, we proposed a new index for assessing LV diastolic function, flow propagation velocity, which can be measured with color M-mode Doppler echocardiography and baseline-shift technique. Recent studies have shown that the flow propagation velocity is a unique noninvasive parameter of LV diastolic function which can accurately detect the diastolic impairment in patients with different types of cardiac diseases with various loading conditions.
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PMID:[Cardiovascular ultrasound: applications for the assessment of cardiac function]. 1139 44

The ECG strain pattern of lateral ST depression and T-wave inversion is a marker for left ventricular hypertrophy (LVH) and adverse prognosis in population studies. However, whether ECG strain is an independent predictor of cardiovascular (CV) morbidity and mortality in the setting of aggressive antihypertensive therapy is unclear. ECGs were examined at study baseline in 8854 hypertensive patients with ECG LVH who were treated in a blinded manner with atenolol- or losartan-based regimens. Strain was defined by the presence of a downsloping convex ST segment with an inverted asymmetrical T wave opposite to the QRS axis in leads V5 and/or V6 and was present in 971 patients (11.0%). The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study composite end point of CV death or nonfatal myocardial infarction or stroke occurred in 1035 patients (11.7%). In Cox analyses adjusting only for treatment effect, ECG strain was a significant predictor of CV death (hazard ratio [HR] 2.26, 95% confidence interval [CI] 1.78 to 2.86), fatal/nonfatal myocardial infarction (HR 2.16, 95% CI 1.67 to 2.80), fatal/nonfatal stroke (HR 1.76, 95% CI 1.39 to 2.21), and the composite CV end point (HR 1.99, 95% CI 1.70 to 2.33). After further adjusting for standard CV risk factors, baseline blood pressure, and severity of ECG LVH, ECG strain remained a significant predictor of CV mortality (HR 1.53, 95% CI 1.18 to 2.00), myocardial infarction (HR 1.55, 95% CI 1.16 to 2.06), and the composite CV end point (HR 1.33, 95% CI 1.11 to 1.59). Thus, ECG strain is a marker of increased CV risk in hypertensive patients in the setting of aggressive blood pressure lowering, independent of baseline severity of ECG LVH.
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PMID:Electrocardiographic strain pattern and prediction of cardiovascular morbidity and mortality in hypertensive patients. 1517 25

Hypertension is a major healthcare problem afflicting nearly 50 million individuals in the United States. Despite its strong causal association with cardiovascular disease complications including myocardial infarction, heart failure, and stroke, the majority of patients with hypertension do not achieve optimal blood pressure control. The prevalence of hypertension is expected to increase with the aging population, growing obesity epidemic, and rising incidence of metabolic syndrome. Endothelial dysfunction and reduced nitric oxide (NO) bioactivity represent prominent pathophysiological abnormalities associated with hypertensive cardiovascular disease. Individuals with hypertension exhibit blunted epicardial and resistance vascular dilation to endothelium-derived nitric oxide (EDNO) agonists in the peripheral and coronary circulation that likely contributes to mechanisms of altered vascular tone in hypertension. The amino acid L-arginine serves as the principal substrate for vascular NO production. Numerous studies, though not uniformly, demonstrate a beneficial effect of acute and chronic L-arginine supplementation on EDNO production and endothelial function, and L-arginine has been shown to reduce systemic blood pressure in some forms of experimental hypertension. This brief review discusses the potential role of L-arginine in hypertension, and reviews possible mechanisms of L-arginine action including modulation of EDNO production, alteration of asymmetrical dimethylarginine (ADMA):L-arginine balance, and possible improvement of insulin sensitivity. In view of the rising prevalence of hypertension, randomized human clinical studies investigating the potential therapeutic role of L-arginine may be warranted.
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PMID:L-arginine and hypertension. 1546 90

Entrapment of lipoprotein particles in the extracellular matrix of the arterial intima is a characteristic feature of the development of atherosclerosis, the disease behind myocardial infarction and stroke. In this study, sugars were exploited in the separation of lipoproteins by CE. Monosaccharides, disaccharides and one sugar alcohol used during ultracentrifugal isolation of lipoproteins prevented the strong and unfavorable adsorption of lipoprotein particles on the capillary wall, allowing their selective separation in uncoated fused silica capillary. The effect of ionic strength of the phosphate BGE solution on the separation at physiological pH was clarified. Asymmetrical flow field-flow fractionation and dynamic light scattering showed that sugars affected the structure of lipoproteins by decreasing their sizes. Although in molecular dynamics simulations, only a 19 amino acid peptide of apolipoprotein B-100 and a 15 amino acid peptide of apolipoprotein E were employed, the results also indicated a decrease in lipoprotein size, supporting the asymmetrical flow field-flow fractionation and dynamic light scattering results.
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PMID:Sugar treatment of human lipoprotein particles and their separation by capillary electrophoresis. 2060 41

Ischemia-reperfusion (IR) was surgically performed in murine hearts which were then subjected to repeated imaging to monitor temporal changes in functional parameters of key clinical significance. Two-dimensional movies were acquired at high frame rate (8 kHz) and were utilized to estimate high-quality myocardial strain. Two-dimensional elastograms (strain images), as well as strain profiles, were visualized. Results were powerful in quantitatively assessing IR-induced changes in cardiac events including left-ventricular (LV) contraction, LV relaxation and isovolumetric phases of both pre-IR and post-IR beating hearts in intact mice. In addition, compromised sector-wise wall motion and anatomical deformation in the infarcted myocardium were visualized. The elastograms were uniquely able to provide information on the following parameters in addition to standard physiological indices that are known to be affected by myocardial infarction in the mouse: internal diameters of mitral valve orifice and aorta, effective regurgitant orifice, myocardial strain (circumferential as well as radial), turbulence in blood flow pattern as revealed by the color Doppler movies and velocity profiles, asynchrony in LV sector, and changes in the length and direction of vectors demonstrating slower and asymmetrical wall movement. This work emphasizes on the visual demonstration of how such analyses are performed.
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PMID:High-frequency high-resolution echocardiography: first evidence on non-invasive repeated measure of myocardial strain, contractility, and mitral regurgitation in the ischemia-reperfused murine heart. 2064 13

Subsequent to myocardial infarction, cardiomyocytes within the infarcted areas and border zones expose phosphatidylserine (PS) in the outer plasma membrane leaflet (flip-flop). We showed earlier that in addition to apoptosis, this flip-flop can be reversible in cardiomyocytes. We now investigated a possible role for Rho and downstream effector Rho-associated kinase (ROCK) in the process of (reversible) PS exposure and apoptosis in cardiomyocytes. In rat cardiomyoblasts (H9c2 cells) and isolated adult ventricular rat cardiomyocytes Clostridium difficile Toxin B (TcdB), a Rho GTPase family inhibitor, C3 transferase (C3), a Rho(A,B,C) inhibitor and the ROCK inhibitors Y27632 and H1152 were used to inhibit Rho-ROCK signaling. PS exposure was assessed via flow cytometry and fluorescent digital imaging microscopy using annexin V. Akt expression and phosphorylation were analyzed via Western blot, and Akt activity was inhibited by wortmannin. The cellular concentration activated caspase 3 was determined as a measure of apoptosis, and flippase activity was assessed via flow cytometry using NBD-labeled PS. TcdB, C3, Y27632 and H1152 all significantly increased PS exposure. TcdB, Y27632 and H1152 all significantly inhibited phosphorylation of the anti-apoptotic protein Akt and Akt inhibition by wortmannin lead to increased PS exposure. However, only TcdB and C3, but not ROCK- or Akt inhibition led to caspase 3 activation and thus apoptosis. Notably, pancaspase inhibitor zVAD only partially inhibited TcdB-induced PS exposure indicating the existence of apoptotic and non-apoptotic PS exposure. The induced PS exposure coincided with decreased flippase activity as measured with NBD-labeled PS flip-flop. In this study, we show a regulatory role for a novel signaling route, Rho-ROCK-flippase signaling, in maintaining asymmetrical membrane phospholipid distribution in cardiomyocytes.
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PMID:Inhibition of Rho-ROCK signaling induces apoptotic and non-apoptotic PS exposure in cardiomyocytes via inhibition of flippase. 2069 98


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