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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Congenital heart disease can predispose individuals to pulmonary vascular remodeling as a result of the abnormality in pulmonary blood flow and pressure that accompanies the specific congenital defect being considered. Pulmonary arterial hypertension associated with congenital heart defects is an important determinant of functional capacity and survival, especially when the Eisenmenger's state of reversed shunt is present. The likelihood of right ventricular dysfunction and failure increases with the degree of pulmonary artery pressure. Thus, the aim of disease management in this patient population should be to prevent or improve right heart failure. Current therapies that modify the progression of pulmonary vascular disease-including endothelin-1 receptor antagonists, phosphodiesterase-5 inhibitors, and prostanoids-should be considered carefully in patients with congenital heart disease-associated pulmonary hypertension. The risks and benefits of altering the balance of pulmonary vascular resistance to systemic vascular resistance must be weighed for each patient.
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PMID:Pulmonary hypertension complicating congenital heart disease. 1956 32

Erectile dysfunction (ED) is a highly prevalent disorder which adversely affects quality of life. The prevalence of erectile dysfunctions affects more than half of the male population over 60 years. Cardiovascular diseases are also highly prevalent conditions and frequently occur concommitantly with ED, mainly because of common several pathophysiological and risk factors. Impressive advances in the management of erectile dysfunction have occurred over the past decade when oral therapy with vasoactive agents has become a first-line treatment. The most widely used class of agents for these kind of disorders is 5-phosphodiesterase inhibitors (5-PDEI). Because the enzyme that they inhibit--PDE-5 is found in smooth muscle cells of the systemic arteries and veins throughout the body, these agents have mild vasodilator effects and thus, have the potential to impact the cardiovascular system. In this article, we review the physiology and the pathophysiology of erection, the influence of 5-PDEI over circulatory system and interactions with drugs commonly used in circulatory disorders. The other purpose of the review (based on the Princeton Consensus I and II) is to present guidelines for safe management of cardiac patients regarding sexual activity and the treatment of ED. We also imply that the recognition of ED is a warning sign of silent vascular disease. Thus a man with ED and no cardiac symptoms may be a cardiac or vascular patient. The conclusion is that, with regard to described rules, PDE-5 inhibitors are safe and effective for the treatment of ED patients with cardiac diseases, including patients with chronic coronary artery disease and hypertension.
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PMID:[The safety of 5-phosphodiesterase inhibitors in the treatment of erectile dysfunction in patients with cardiovascular disease]. 1970 9

Patients with systemic sclerosis (SSc) can develop pulmonary hypertension (PH; mean pulmonary artery pressure >/= 25 mm Hg) caused by pulmonary arterial hypertension (PAH), left ventricular disease, or pulmonary fibrosis. PAH is a pulmonary vascular disease, the diagnosis of which requires pulmonary capillary wedge pressure less than 15 mm Hg, pulmonary vascular resistance greater than 3 Wood Units, and exclusion of thromboembolism and parenchymal lung disease. Molecular mechanisms underlying PAH-SSc include activation of inflammatory and fibrogenic pathways in the vasculature and right ventricle. Circulating autoantibodies trigger endothelial damage and fibroblast activation. PAH most commonly occurs as a late complication in patients with limited cutaneous disease and anticentromere antibodies. Although echocardiography is a useful screening tool, heart catheterization is required to diagnose PAH before initiating therapy. Prognosis and therapeutic response are worse in PAH-SSc than in other PAH categories (median survival, 1-3 y). Approved therapies include prostacyclins, endothelin antagonists, and phosphodiesterase type 5 inhibitors. Research is needed to define disease mechanisms and develop effective therapies.
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PMID:Diagnosis and management of pulmonary hypertension in systemic sclerosis. 2042 28

Pulmonary thromboendarterectomy is the treatment of choice in patients with chronic thromboembolic pulmonary hypertension (CTEPH). However, specific medical treatment of pulmonary hypertension (PH) can be an alternative or play a complementary role to surgery. Thus, in patients unsuitable for surgery due to distal thrombotic obstruction, residual or persistent PH after surgery or very severe PH and a high-risk hemodynamic profile, medical treatment may improve their clinical course and the outcome of thromboendarterectomy. Patients with distal obstruction in the pulmonary tree and those with residual PH after surgery show clinical and hemodynamic deterioration due to progression of the pulmonary vascular disease in the smallcaliber arterioles. Conventional treatment with diuretics, anticoagulants and oxygen therapy has been demonstrated to have little effectiveness. In the last decade, numerous drugs have been developed for the treatment of PH: prostacyclin analogs, endothelin receptor antagonists, and phosphodiesterase-5 inhibitors acting principally in vascular remodelling of small-caliber arterioles. Although evidence of the effectiveness of these drugs in PH and the histological similarity of small-vessel vasculopathy in CTEPH to that of other forms of PH provide the main rationale for the use of these drugs in patients with CTEPH, the evidence from clinical trials is still limited.
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PMID:[Medical treatment in patients with chronic thromboembolic pulmonary hypertension]. 2054 99

Causes of pulmonary arterial hypertension (PAH) are similar in adults and children. The main difference is that PAH secondary to congenital heart diseases, is the predominant cause in pediatric patients. Persistent pulmonary hypertension of the newborn shows completely different clinical course and pathophysiological mechanisms. It is usually seen in full term babies with a high morbidity and mortality rate. Improved prognosis has been reported with inhaled nitric oxide (NO) and extracorporeal membrane oxygenation therapy in babies hospitalized in well equipped and experienced newborn centers. Primary pulmonary hypertension and familial pulmonary hypertension are rare in pediatric age group because the diagnosis is initially made in adolescence. The incidence of PAH secondary to congenital heart disease is estimated as 1.6 - 12.5 case/million/year. Eisenmenger syndrome is diagnosed in 1% of patients with PAH. Patients with left to right shunts are the main group who develop pulmonary vascular disease if not treated in the early infancy. Some cyanotic congenital heart diseases are also the causes of PAH. The best treatment of patients at risk for the development of pulmonary vascular disease is prevention by early surgical elimination of defects or repairing the anatomy. Treatment options with vasodilating agents like NO, prostaglandin analogs, phosphodiesterase -5 inhibitors and endothelin receptor antagonists are used to improve survival and quality of life. Heart lung or bilateral lung transplantation is the only surgical option for many of these patients. Results of national and international registries will bring valuable epidemiological and prognostic perspectives to pediatric PAH.
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PMID:[Pediatric pulmonary hypertension and pulmonary arterial hypertension secondary to congenital heart diseases]. 2081 67

Pulmonary arterial hypertension (PAH) commonly arises in patients with congenital heart disease (CHD). Greater numbers of patients with PAH associated with CHD (PAH-CHD) are now surviving into adulthood, many with increasingly complex cardiac defects. Patients with cardiac defects which result in left-to-right shunting are at risk of developing PAH, owing to the increased shear stress and circumferential stretch induced by increased pulmonary blood flow, which leads to endothelial dysfunction and progressive vascular remodelling and, thus, increased pulmonary vascular resistance. Although PAH-CHD shares similar lung histology with idiopathic PAH, differences do exist between these aetiologies. Management of PAH-CHD can involve surgical correction of the cardiac defect and/or treatment of the PAH, depending on the underlying cardiac defect and status of disease progression. Transplantation surgery can be curative but is not without limitations. The timing of intervention in patients with PAH-CHD is important, but the optimums are sometimes difficult to define, with limited robust data to inform management decisions. Uncontrolled studies suggest that prostacyclin analogues and phosphodiesterase type-5 inhibitors may have benefits in advanced pulmonary vascular disease. In the only randomised controlled trial dedicated to end-stage PAH-CHD, bosentan significantly reduced pulmonary vascular resistance and significantly increased 6-minute walk distance without compromising peripheral oxygen saturation, in patients with Eisenmenger syndrome. These data suggest that targeted therapies are beneficial in the PAH-CHD population, and warrant further research.
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PMID:Pulmonary arterial hypertension in paediatric and adult patients with congenital heart disease. 2095 36

The management of erectile dysfunction (ED) has been revolutionized by the discovery of phosphodiesterase 5 (PDE5) inhibitors, which have been commercially available for more than a decade and are the first-line therapeutic option for men with ED. Sildenafil, vardenafil and tadalafil were approved by the European Medicine Agency and the US FDA for the treatment of ED on the back of their high efficacy rates and favorable safety profiles. However, despite the fact that more than 50 million patients with ED worldwide have been successfully treated with one of these PDE5 inhibitors, some men--most notably those with severe neurologic damage, diabetes mellitus or severe vascular disease--are resistant to the currently available drugs and require more-invasive treatments, such as intracavernosal injection therapy. Partly as a consequence of this, research into alternative therapeutic approaches continues, including the development of new PDE5 inhibitors, centrally acting pharmaceutical agents, and application of molecular technologies such as gene therapy and stem cell therapy.
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PMID:An update on new oral PDE5 inhibitors for the treatment of erectile dysfunction. 2106 61

In this article we focus on the pathogenesis and clinical characteristics of schistosomiasis infection on the lung vasculature. Overall, the basic biology and understanding of Schistosoma immune responses and their effect on the cardiopulmonary system is limited in both animal and human models, which hinders clinical care and drug development. The inflammatory response to the eggs in the lung appears to contribute to the remodeling of the pulmonary vessels. Portal hypertension caused by parasitemia also appears to contribute to the development of pathophysiologic alterations of the pulmonary vascular bed. Antischistosomal therapy, praziquantel, used for pulmonary hypertension secondary to schistosomiasis usually has no effect, but it is given to prevent further progression of disease. Currently, there are no clinical trials for the treatment of pulmonary vascular disease secondary to schistosomiasis. Specialty drugs such as phosphodiesterase type 5 or tyrosine kinase inhibitors exhibit some interesting activity, yet are prohibitively expensive, lack safety and efficacy studies in schistosomiasis endemic populations, and tend to be limited by safety, efficacy, route of administration and compliance problems.
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PMID:Pulmonary vascular disease associated with schistosomiasis. 2113 70

Lifestyle and nutrition have been increasingly recognized as central factors influencing vascular nitric oxide (NO) production and erectile function. This review underscores the importance of NO as the principal mediator influencing cardiovascular health and erectile function. Erectile dysfunction (ED) is associated with smoking, excessive alcohol intake, physical inactivity, abdominal obesity, diabetes, hypertension, and decreased antioxidant defenses, all of which reduce NO production. Better lifestyle choices; physical exercise; improved nutrition and weight control; adequate intake of or supplementation with omega-3 fatty acids, antioxidants, calcium, and folic acid; and replacement of any testosterone deficiency will all improve vascular and erectile function and the response to phosphodiesterase-5 inhibitors, which also increase vascular NO production. More frequent penile-specific exercise improves local endothelial NO production. Excessive intake of vitamin E, calcium, l-arginine, or l-citrulline may impart significant cardiovascular risks. Interventions discussed also lower blood pressure or prevent hypertension. Certain angiotensin II receptor blockers improve erectile function and reduce oxidative stress. In men aged <60 years and in men with diabetes or hypertension, erectile dysfunction can be a critical warning sign for existing or impending cardiovascular disease and risk for death. The antiarrhythmic effect of omega-3 fatty acids may be particularly crucial for these men at greatest risk for sudden death. In conclusion, by better understanding the complex factors influencing erectile and overall vascular health, physicians can help their patients prevent vascular disease and improve erectile function, which provides more immediate motivation for men to improve their lifestyle habits and cardiovascular health.
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PMID:The link between erectile and cardiovascular health: the canary in the coal mine. 2162 50

Pulmonary arterial hypertension (PAH) develops from an abnormal interaction between the endothelium and smooth muscle cells in the pulmonary vasculature and is characterized by a progressive rise in pulmonary vascular resistance resulting from vascular remodeling, vasoconstriction, and cellular proliferation. Currently, 3 classes of drugs are approved for the treatment of PAH based on results from small short-term clinical trials-prostacyclin analogues, endothelin receptor antagonists, and phosphodiesterase type 5 inhibitors. The pharmacologic management of PAH is rapidly evolving as newer therapeutic targets that stabilize or reverse pulmonary vascular disease and target right ventricular function are being sought and as clinical practice patterns shift in favor of earlier diagnosis and aggressive treatment. This manuscript will review the practical management aspects of currently approved PAH treatments and briefly discuss combination therapy and novel pharmacologic targets. In addition, the treatment of acute right ventricular failure and evidence (or lack thereof) for therapies in non-PAH pulmonary hypertension, such as pulmonary hypertension from left side of the heart disease, are addressed.
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PMID:Current therapeutics and practical management strategies for pulmonary arterial hypertension. 2183 79


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