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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A method for the quantitative and qualitative determination of the number of aggregated platelets is described. One milliliter of venous blood was separated equally into two solutions. One solution composed of EDTA (ethylenediaminetetraacetic acid) and formaldehyde (solution F) contained reversibly and irreversibly aggregated platelets, and the second solution, composed of EDTA alone (solution E), contained irreversibly aggregated platelets. By microscopic readings, the percentage of platelets forming aggregates was determined. Reversibly aggregated platelets were estimated by subtracting the percentage of aggregated platelets in solution E from that in solution F. The average amount of platelets per aggregate was calculated by dividing the number of aggregated platelets in solution F by the number of aggregates per 1000 platelets counted. The reference ranges (means +/- SDs) established in 100 healthy persons were 5.8% +/- 2.4% (1% to 9%) for solution F, 3.9% +/- 1.8% (0% to 7%) for solution E, and 2.2 +/- 0.18 (2.0 to 2.5) for the average number of platelets per aggregate. Twenty hospitalized patients without heart disease had values similar to those of 100 normal subjects. In 50 patients with acute myocardial infarction, the percentage of aggregated platelets in solution F was 23.8% +/- 10.3%; in solution E, 4.0% +/- 3.0%; and the average number of platelets per aggregate, 2.9 +/- 0.7. The mean variance for five daily consecutive measurements was 0.52% for solution F, 0.63% for solution E, and 0.002 for the average number of platelets per aggregate. An even lesser mean variance was observed when the interobserver-vs-intraobserver and the intersmear-vs-intrasmear variations were tested. In patients with acute myocardial infarction, the interobserver-vs-intraobserver variance was 5.6% for solution F, 2.2% for solution E, and 0.005 for the average number of platelets per aggregate. The parameters studied were unaffected by different blood drawings, assay tubes, or venous stasis. In 80 patients with unstable angina, the studied parameters as well as the percentage of "big" platelets were measured on hospital days 1, 2, and 5. In 25 patients in whom acute myocardial infarction developed during hospitalization, the percentage of aggregated platelets was 28.1% +/- 8.3%. Most of them (71%) were reversibly aggregated and did not change during hospitalization. The average number of platelets per aggregate was 3.9 +/- 1.6, and the percentage of big platelets was 12.5% +/- 7.2%, both values not undergoing subsequent changes. In patients in whom acute myocardial infarction did not develop, the percentage of aggregated platelets decreased to 14.2% +/- 6.1% on day 5. Most aggregated platelets (58.8% to 90%) were irreversibly aggregated.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A method for the determination of circulating aggregated platelets and its application to patients in the course of unstable angina. 229 67

Study of the microcirculation primarily involves assessment of the capillaroscopic findings. In the clinical field, these are mainly obtained from small vessels of the conjunctiva and nail bed. In more recent years, microcirculation has been accompanied as a subject of examination by haemorheology. The study of blood viscosity and red cell deformability is the most promising from the practical standpoint. In the diagnostic and physiopathological evaluation of capillaroscopic findings, importance is attached to differentiation of arterial and venous vessels, the size, shape and configuration of the small vessels, and above all the presence of intravasal red cell clumps. In examination of the nail bed, particular attention is directed to oddities in the shape of the capillary loops, venous stasis and congestion pictures (in decompensated heart disease, for example, and in cor pulmonale), and alterations in the subpapillary plexuses. Examination of the conjunctiva takes account of the presence of tortuous and serpiginous vessels, with pronounced dilatations, as observed in cardiocirculatory decompensation and chronic bronchopulmonary diseases. In arteriosclerosis, tortuosity and dilatation, even as far as the formation of microaneurysms, may be accompanied by the percent of stiff, thin vessels in networks or webs of various sizes. Clinical pharmacology tests, such as those employing vasoactive drugs (xanthinol nicotinate, buflomedyl, cyticholine) are of interest. They result in a marked increase in calibre, with the appearance of collaterals, regression of red cell aggregates, and improved blood flow.
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PMID:[Microcirculation in the conjunctiva and the nail bed in the aged. Symptomatic and clinico-pharmacologic aspects]. 717 57

Several health hazards and social disabilities are associated with obesity. Increased mortality is associated with increased body weight. A high rate of mortality results from heart disease, diabetes mellitus, gallbladder disease, high blood pressure, and cancer. Physiologic cardiovascular changes occur, leading to left ventricular hypertrophy and lipid abnormalities. Hypertension, stroke, and venous stasis are increased. Pulmonary abnormalities include obstructive sleep apnea, which can be associated with secondary polycythemia and right ventricular hypertrophy. Gallstones, gallbladder disease, and accumulation of fat on the liver are significantly increased. Gout and reproductive abnormalities in women are common. Osteoarthritis of the knees and spine occur, although osteoporosis is rare. Risk for endometrial and breast cancer is increased, particularly in the presence of increased central fat. Changes in the skin include stretch marks, acanthosis negricans, hirsutism, intertrigo, and multiple papillomas. Impaired psychosocial function is manifested as social isolation, loss of job mobility, increased employee absenteeism, and economic and social discrimination.
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PMID:Health hazards of obesity. 897 52

Venous thromboembolism is a common and potentially lethal disease. Patients who have pulmonary embolism are at especially high risk for death. Death owing to pulmonary embolism is independent of other comorbid conditions (e.g., cancer, chronic heart disease, or lung disease). Sudden death is often the first clinical manifestation. Only a reduction in the incidence of venous thromboembolism can reduce sudden death owing to pulmonary embolism and venous stasis syndrome owing to deep vein thrombosis. The incidence of venous thromboembolism has been relatively constant since about 1980. Improvement in the incidence of venous thromboembolism will require better recognition of persons at risk, improved estimates of the magnitude of risk, the avoidance of risk exposure when possible, more widespread use of safe and effective prophylaxis when risk is unavoidable, and targeting of prophylaxis to those persons who will benefit most. Recognition of venous thromboembolism as a multifactorial disease with genetic and genetic-environmental interaction has provided significant insights into its epidemiology and offers the possibility of improved identification of persons at risk for incident and recurrent venous thromboembolism.
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PMID:Risk factors for venous thromboembolism. 1268 52

Congenital absence of the inferior vena cava (CAIVC) is a rare vascular defect, commonly reported as a fortuitous finding because patients are typically asymptomatic of the condition itself but are symptomatic of associated conditions such as congenital heart disease, polysplenia, asplenia, and inversion of bowel viscera. The presence of CAIVC is probably underestimated because CAIVC may not be detected by compression B-mode ultrasonography. By use of computed tomography, we diagnosed a case of CAIVC in a young athletic patient with disabling venous stasis symptoms of the lower limbs. Venous prosthetic reconstruction of the infrarenal vena cava provided with early subsiding of edema and healing of stasis ulcers. An intracaval web was found as potentially responsible for the condition. We present and propose our surgical method for this rare disabling condition.
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PMID:Surgical management of deep venous insufficiency caused by congenital absence of the infrarenal inferior vena cava. 1823 69

Prostaglandin E1 (PGE1) is the drug of choice for providing ductal patency in cyanotic congenital heart disease (CCHD) for a short period of time until essential surgical management. Occasionally, prolonged use of PGE1 is required when the surgical procedure is delayed due to certain clinical conditions. Prolonged use of PGE1 may lead to bone and tissue changes such as pretibial and soft tissue swelling of the extremities and reversible cortical proliferation of the bones. Venous stasis as an additional risk factor can result in generalized periosteal reaction that initially can cause the separation of the periosteum from the cortex. We report an infant with CCHD who developed severe tissue swelling and generalized periosteal reaction due to coexistence of prolonged use of PGE1 and venous stasis. To the best of our knowledge, this is the first case report with both of these risk factors.
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PMID:Generalized periosteal reaction and tissue swelling secondary to prolonged prostaglandin E1 infusion and venous stasis: a case report. 2438 39

Isolated severe tricuspid valve stenosis due to an endocardial pacemaker lead is extremely rare, and is usually caused by either fibrosis of a perforated or lacerated leaflet, or fibrotic adherence between the lead and the valvular apparatus. Reported cases typically include clinical manifestations of both systemic venous stasis and low cardiac output. The case is presented of a 20-year-old female with a surgically repaired congenital heart disease who developed severe tricuspid stenosis at six years after the implantation of a DDD pacemaker. Unexpectedly, the patient had no signs of venous stasis and suffered only from exercise intolerance. Right heart catheterization under fluoroscopic guidance revealed an atrial lead forming a loop at the level of the tricuspid valve. A paradoxical inspiratory decrease in the transvalvular diastolic gradient, caused by the caudal heart motion and straightening of the loop during inspiration, was noted. Such a dynamic nature with a temporary inspiratory relief of the obstruction may explain the partial clinical presentation of tricuspid stenosis in this case. The lead was removed and the tricuspid valve repaired surgically, after which the patient's recovery was uneventful with normalization of exercise tolerance.
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PMID:Dynamic tricuspid valve stenosis induced with a pacemaker lead: a case report. 2477 42

Adults with congenital heart disease who underwent the Fontan operation to palliate single ventricle heart defects-by direct connection of caval venous return to the pulmonary circulation-have improved survival due to advancements in surgical and interventional techniques. However, cardiac and non-cardiac comorbidities often coexist, complicating management, and contributing to premature morbidity and mortality. Cardiac issues include heart failure symptoms related to systolic and diastolic dysfunction, atrial and ventricular arrhythmias and systemic atrioventricular valve regurgitation. Structural issues may be related to obstruction of the Fontan pathway, or to branch pulmonary artery stenosis, both of which exacerbate symptoms. Non-cardiac complications in adults involve hepatic congestion, fibrosis and cirrhosis, hepatocellular carcinoma, chronic kidney disease, stroke, venous stasis, lymphatic issues and involvement of other organ systems. 'Fontan failure' refers to circulatory dysfunction, either cardiac, non-cardiac, or both, diagnosed after exclusion or treatment of reversible contributors such as structural issues and arrhythmias. Counselling about reproductive health, mental health, perioperative management and overall wellness are paramount for patients' well-being. Fontan patients are typically managed in highly specialised adult congenital heart centres, but may present to cardiologists or other practitioners with cardiac and non-cardiac emergencies or urgencies, sometimes after being out of care. In this review, we discuss the management of the adult Fontan patient, including surveillance, cardiac and non-cardiac complications, reproductive health, and advanced therapies.
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PMID:Management of the adult Fontan patient. 3166 32

Renal congestion is becoming recognized as a potential contributor to cardiorenal syndromes. Adequate control of congestion with simultaneous preservation of renal function has been proposed as a central goal of the management of heart failure. We report our care of a 48-year-old woman suffering from right heart failure and massive fluid overload due to severe pulmonary hypertension secondary to a combination of left-heart disease and status after recurrent pulmonary embolisms. Alterations in Doppler-derived intrarenal venous flow patterns and a novel renal venous stasis index were used to evaluate improvement in renal venous congestion during recompensation. Due to refractory congestion despite optimal medical treatment and continuous veno-venous hemodialysis, a peritoneal dialysis catheter was placed to relieve the massive ascites. The paracentesis of ascites led to a significant loss of weight, normalization of hydration status with subsequent termination of continuous veno-venous hemodialysis, and a significant improvement in clinical and echocardiographic parameters. Renal Doppler ultrasonography showed continuous improvement in intrarenal venous flow patterns and the renal venous stasis index indicative of effective decongestion up to a normal intrarenal venous flow pattern and renal venous stasis index. Furthermore, residual renal function increased during follow-up. This case demonstrates the feasibility of renal Doppler ultrasonography as a simple, non-invasive, and integrative measure of renal congestion. The renal venous stasis index and intrarenal venous flow patterns may be useful to evaluate the treatment response and to guide therapy in patients with right heart failure.
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PMID:Alterations in Doppler-derived renal venous stasis index during recompensation of right heart failure and fluid overload in a patient with pulmonary hypertension. 3191 17