Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the effect of Kawasaki syndrome on myocardial function, as well as the influence of high-dose intravenous gamma-globulin therapy on resolution of functional abnormalities, we studied 98 patients with Kawasaki syndrome during five time intervals from onset of illness: 1) 10 days or less, 2) 11-31 days, 3) 1-3 months, 4) 3-12 months, and 5) 1-3 years. Normal controls included 48 children under age 8 years, without known cardiovascular disease. Using two-dimensional directed M-mode echocardiograms, we obtained chamber dimensions, fractional shortening, rate-corrected velocity of shortening (Vcfc) adjusted for end-systolic wall stress, and early diastolic function parameters that included adjusted peak rates of left ventricular dimension change, wall thinning, and their respective timing. Left ventricular systolic and diastolic dimensions were larger (both p less than 0.01) in patients than in normal subjects in period 1. Stress-adjusted Vcfc was much lower in patients in the 3 months after disease onset; by period 5, contractility was comparable in patients and normal subjects. Adjusted indexes of early diastolic function did not differ significantly between patients and normal subjects. To investigate the effect of gamma-globulin, we analyzed data on 47 patients prospectively randomized to therapy with aspirin alone (n = 19, 40%) or to aspirin plus gamma-globulin, 400 mg/kg/day for 4 consecutive days (n = 28, 60%). In period 1, before treatment, the two groups had mean fractional shortening and stress-adjusted Vcfc comparable to each other but much lower than those of normal subjects (p less than or equal to 0.001). Patients treated with aspirin alone continued to have diminished fractional shortening and Vcfc compared with normal subjects in periods 2, 3, and 4 (all p less than or equal to 0.05). In contrast, fractional shortening and Vcfc in gamma-globulin-treated patients in these periods were comparable to those of normal subjects. By period 5, no difference was detected in systolic function or contractility between either treatment group and normal subjects. We conclude that early abnormalities of left ventricular contractility and myocardial function, as assessed by echocardiography, generally resolve by 1-3 years after disease onset and that recovery is accelerated by administration of IVGG in the acute phase.
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PMID:Left ventricular contractility and function in Kawasaki syndrome. Effect of intravenous gamma-globulin. 272 Sep 25

This review outlines the findings associated with topical minoxidil use. Approximately one-third of the treated patients will obtain terminal hair growth using a 2 to 3% solution twice a day. Patients should receive treatment for a minimum of six months to evaluate the drug's efficacy. Factors associated with patients who obtained new hair growth include: a thinning versus absolute baldness, treatment initiated at a relatively younger age, and hair growth noted within three months. Following a positive growth response, there may be a reduction in new hair growth gained with minoxidil use for more than one year. Stopping the medication is associated with an exacerbation of hair loss. Currently, patients with hypertension, cardiovascular disease, or any serious systemic illness should be excluded from therapy. Patients should be monitored every four to six months, or sooner with any complaints. Initial evaluation should include monitoring of the blood pressure, pulse, electrocardiogram and serum lipid determinations.
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PMID:Topical minoxidil: its use in treatment of male pattern baldness. 306 59

Gated magnetic resonance (MR) imaging was used to evaluate central cardiovascular anatomy in 172 subjects, 31 of whom were healthy volunteers. Using the spin-echo technique, images of diagnostic quality were obtained in 93% of cases with TE = 28 msec and in 65% of cases with TE = 56 msec. Transverse multisection sequences encompassing most of the left ventricle required approximately 6-8 minutes. Corroborative studies were available in 134 of 141 patients who had cardiovascular disease; two dimensional echocardiograms and angiography in 133 and 100 patients, respectively. Gated MR demonstrated the wall thinning and complications caused by prior myocardial infarctions and high signal intensity of the myocardium at the site of acute myocardial infarctions. MR accurately demonstrated anatomic abnormalities owing to hypertrophic and congestive cardiomyopathies, congenital abnormalities of the heart and great vessels, rheumatic heart disease, pulmonary hypertension, and cardiac and paracardiac masses. Depiction of cardiovascular anatomy and pathoanatomy was attained without the use of any contrast media. Consequently, gated MR is an effective technique for cardiac diagnosis. The short time required for tomographic examination of the entire heart using the multisection technique renders this a practical cardiac imaging modality.
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PMID:Magnetic resonance imaging of the heart: a review of the experience in 172 subjects. 315 39

Fifteen selected hypothyroid patients without symptoms or signs of cardiovascular disease and an equal number of matched control subjects underwent simultaneous recording of electrocardiogram and phono-, apex-, and echocardiography to assess dynamic systolic and diastolic left ventricular function. Both the systolic preejection period and the isovolumic relaxation period were significantly increased in the hypothyroid group. However, whereas the rate of myocardial contraction, assessed from the echocardiograph of the left ventricular posterior wall, was identical in patients and control subjects, the diastolic thinning rate of the muscle was markedly slowed in the hypothyroid individuals. The abnormalities demonstrated were in the main completely reversed after 3 months of T4 therapy. These results demonstrate a relatively selective and readily reversible disturbance of the rate of myocardial relaxation in hypothyroidism, suggesting an intrinsic abnormality of cardiac muscle. This allows an intriguing parallel to be drawn with the delayed relaxation phase of voluntary muscle contraction, long recognized as a direct measure of tissue thyroid function in hypothyroidism. The abnormality of diastolic function we have described is of similar character to that found in patients with other cardiomyopathies and which has been shown to be a major cause of disturbance of global cardiac action.
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PMID:Reversible abnormalities of myocardial relaxation in hypothyroidism. 400 7

A collagen network, composed largely of type I and III fibrillar collagens, is found in the extracellular space of the myocardium. This network has multiple functions which includes a preservation of tissue architecture and chamber geometry. Given its tensile strength, collagen is a major determinant of tissue stiffness. Its disproportionate accumulation, in the form of either a reactive or a reparative fibrosis, further increases stiffness. A degradation of collagen tethers, on the other hand, is an anatomic requisite for a distortion in tissue architecture and a reduction in stiffness that can lead to chamber dilatation, wall thinning, and even rupture of the myocardium. Collagen turnover in the myocardium is dynamic. When synthesis exceeds degradation, an adverse accumulation of collagen appears to distort tissue structure. This is true for either the hypertrophied and/or nonhypertrophied ventricle. Factors that contribute to the appearance of myocardial fibrosis are largely different from those that promote cardiac myocyte growth. Included amongst these fibrogenic factors are effector hormones of the reinin-angiotensin-aldosterone system (RAAS). Studies conducted both in intact animals (relative to dietary sodium intake) and in cultured adult cardiac fibroblasts have pointed toward the association between collagen accumulation and chronic elevations in circulating angiotensin II and aldosterone. A tissue hormonal system involving angiotensin II, endothelins and bradykinin, may likewise regulate fibrogenesis. In this regard, angiotensin converting enzyme is found in connective tissue of the normal heart, including the matrix of heart valves and the adventitia of the intramural coronary arteries, and fibrous tissue that forms following infarction or with chronic RAAS activation. The importance of ACE in the regulation of local angiotensin II and bradykinin levels and their contribution to collagen turnover is a fruitful area of research with important clinical implications. The myocardium also contains a proteolytic system, including collagenase. The characteristics and regulation of matrix metalloproteinases and their tissue inhibitors in various cardiovascular disease states requires further investigation.
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PMID:Collagen network of the myocardium: function, structural remodeling and regulatory mechanisms. 802 11

Although cardiomyocyte damage is normally irreversible, gene therapy and somatic cell transfer offer potential for improving function in damaged regions of the heart. However, in ischemic models of injury, variability in depth, size, and location of damage compromises statistical evaluation of in vivo function. We have adapted cryoablation to create a reproducible, posterior, transmural lesion within rabbit myocardium in which small changes in function are measurable in vivo. Before and at 2 and 6 wk postinjury, in vivo left ventricular intracavitary pressure and myocardial segment length were measured. Regional indexes of performance, segmental stroke work (SW), and percent systolic shortening (SS) were significantly decreased (P < 0.001) postcryoinjury as was the slope (Mw) of the linear preload recruitable SW relationship between SW and end-diastolic segment length (P = 0.0001). Decreased SW, SS, and Mw correlated with wall thinning, loss of myocytes, presence of fibroblasts, and transmural scar formation. Reproducible changes in regional myocardial performance in vivo postcryoinjury suggest that this is a reasonable model for evaluating novel therapies for cardiovascular disease.
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PMID:A load-independent in vivo model for evaluating therapeutic interventions in injured myocardium. 981 92

In three patients, a 36-year-old HIV seropositive homosexual man and two women aged 35 and 59 years who had acquired HIV infection through heterosexual contact, signs of lipodystrophy developed after prolonged anti-HIV triple therapy. The observed syndrome is seen after prolonged use of HIV protease inhibitors: it is characterized by peripheral fat wasting, central fat accumulation, hyperlipidaemia and insulin resistance. Typically the subcutaneous fatty tissue disappears resulting in prominent zygomata, veins and muscles and thinning of extremities and buttocks. In addition to abdominal fat accumulation, there have been reports on the occurrence of a dorsocervical fat pad, the so-called buffalo hump. Lipodystrophy caused by protease inhibitors is a risk factor for cardiovascular disease. Recognition of the syndrome is essential for adequate follow-up and possible treatment.
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PMID:[Lipodystrophy and 'buffalo hump' during treatment with HIV protease inhibitors]. 1006 60

Atherosclerotic plaques were likened histologically to healing inflammatory lesions by Russell Ross, who proposed a "response to injury" hypothesis for their formation. More recently, intraplaque inflammation has been postulated to play a role in thinning of the fibrous cap, plaque rupture, and superadded thrombosis. Potential causes for vascular injury include mechanical stress, smoke exposure, hypercholesterolemia, hyperhomocysteinemia, and chronic infection (direct, or indirect). Blood levels of inflammatory markers (e.g., C-reactive protein [CRP]; serum amyloid A [SAA]; fibrinogen; plasma viscosity; erythrocyte sedimentation rate [ESR]; leukocyte count, low serum albumin) have been associated with vascular risk factors and with prevalent and incident atherothrombotic cardiovascular disease (CVD) (coronary heart disease, [CHD]; stroke; and peripheral arterial disease). More recently, cytokines (e.g., interleukin-6 [IL-6]) and soluble adhesion molecules (e.g., intercellular adhesion molecule-1, vascular cell adhesion molecule-1) have been associated with both risk factors and disease; and offer potential therapeutic targets for nonspecific "anti-inflammatory" treatment of arterial disease. Infections associated with arterial disease include specific infections (Chlamydia pneumoniae, Helicobacter pylori) and nonspecific infections (periodontal infections, respiratory tract infections). Recent meta-analyses have shown that associations of serum markers of C. pneumoniae and H. pylori with arterial disease, risk factors, or potential intermediary mechanisms for disease are weaker than was first suggested by early reports. Likewise, further studies and meta-analyses are required to evaluate the epidemiologic relationships of CVD to periodontal infection and disease and to chronic pulmonary infections and disease. The weaker the associations between chronic infections and CVD, the larger is the size of randomized controlled trials required to establish (or exclude) a preventive effect of infection treatment. While control of chronic infection in the mouth, stomach or lungs is appropriate for its local effects, proving its efficacy in prevention of CVD presents a continuing challenge to medical science.
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PMID:The relationship between infection, inflammation, and cardiovascular disease: an overview. 1188 52

Enhanced platelet function, particularly in response to collagen, is a common occurrence in diabetes that increases the risk of cardiovascular disease. Ginkgo biloba extract is ingested primarily to improve mental focus but it possesses a blood-thinning potential, which has not been well characterized. This study was designed to compare the effect of ingesting G. biloba extract on platelet aggregation in platelet-rich plasma (PRP) and prostanoid urinary excretion in healthy volunteers and subjects with Type 2 diabetes mellitus (T2DM). Before and after ingesting 120 mg of standardized G. biloba extract for 3 months, platelet aggregation was studied in PRP and urinary metabolites of thromboxane B(2) (TXB(2)) and prostacyclin (PGI(2)) were measured. In healthy volunteers (age, 42+/-11 years; BMI, 28.4+/-4.8 kg/m(2); n=28), the ingestion of G. biloba extract significantly increased fasting insulin and C-peptide (10+/-4 vs. 12+/-6 microU/ml, p<0.007 and 1.3+/-0.8 vs. 2.1+/-1.1 ng/ml, p<0.001, respectively) and significantly reduced collagen but not PAF-mediated platelet aggregation, converting 21 of 28 subjects with [COL+/EPI+] platelets to the [COL-/EPI+] phenotype. This was accompanied by a reduction of 11-dehydro-TXB(2) from 12.4+/-6.1 to 10.3+/-6.1 ng/mg Cr (p<0.04) and PGI(2) metabolites (2,3-dinor-6-keto-PGF(1alpha) and 6-keto-PGF(1alpha)) from 2.2+/-0.8 to 1.8+/-0.8 ng/mg Cr (p<0.05). In the T2DM subjects (age, 54+/-8; BMI, 36.6+/-7.9 kg/m(2); n=19), G. biloba ingestion did not affect pancreatic beta-cell function but significantly reduced platelet aggregation, converting 16 of 19 [COL+/EPI+] platelets to the [COL-/EPI+] phenotype. Unlike the healthy volunteers, this was not accompanied by a reduced urinary prostanoid excretion. G. biloba-induced reduction of both classes of prostanoid metabolites in healthy volunteers, but not in T2DM subjects, may suggest a nonselective inhibition of COX-1-mediated TXA(2) in platelets and COX-2-mediated PGI(2) production by the endothelial cells and perhaps platelet-enriched levels of arachidonic acid or COX-1 activity, or both, in T2DM subjects.
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PMID:Effect of the ingestion of Ginkgo biloba extract on platelet aggregation and urinary prostanoid excretion in healthy and Type 2 diabetic subjects. 1259 Sep 52

The arterial content of hyaluronan (HA) undergoes diffuse changes as part of the diabetic macroangiopathy. Because HA influences the phenotype of vascular cells in vitro such as proliferation, migration, and secretion, it is tempting to speculate that diabetes-induced hastened cardiovascular disease may be linked to the increased amount of HA. To explore the pathophysiological role of altered HA content in the arterial wall in vivo, we created transgenic (Tg) mice with HA overexpression in smooth muscle cells (SMCs) in large and small vessels, targeted by the alpha smooth-muscle-cell-actin (alphaSMA) promoter fused to the human hyaluronan synthase 2 (hHAS2) cDNA. RT-PCR demonstrated hHAS2 mRNA expression in the tunica media of large and small vessels. In situ hybridization confirmed that hHAS2 mRNA was targeted to the SMCs. The aortic HA content was elevated in the Tg mice, and by immunohistochemistry, it was seen that HA accumulated in the tunica media. The secretory profile of high- and low-molecular HA was similar in wild-type and Tg animals. Overproduction of HA in the aorta resulted in thinning of the elastic lamellae in Tg mice. Our data suggest that this may lead to increased mechanical stiffness and strength, as determined by controlled stretching until failure. Finally, overproduction of HA on the genetic background of the ApoE-deficient mouse strain promoted atherosclerosis development in the aorta. These results indicate that a single component of the diabetic macroangiopathy, diffuse accumulation of HA, accelerates the progression of atherosclerosis.
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PMID:Overexpression of hyaluronan in the tunica media promotes the development of atherosclerosis. 1570 63


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