Rastelli procedure

The Rastelli procedure is an open heart surgical procedure developed by Italian physician and cardiac surgery researcher, Giancarlo Rastelli in 1967 at the Mayo Clinic and involves using a pulmonary or aortic homograft conduit to relieve pulmonary obstruction in double outlet right ventricle with pulmonary stenosis. It is used to correct certain combinations of congenital heart defects (CHDs): The Rastelli procedure is typically performed between one and two years of age. Since d-TGA, overriding aorta, and DORV are cyanotic heart defects, the child is palliated with a Blalock-Taussig shunt in the meantime.

T-cadherin

CDH13T-cadherin - CDH13
Expression of T-cadherin is upregulated in atherosclerotic lesions and post-angioplasty restenosis —conditions associated with pathological angiogenesis. T-cadherin expression is upregulated in ECs, pericytes and VSMC of atherosclerotic lesions. T-cadherin expression in arterial wall after balloon angioplasty correlates with late stages of neointima formation and coincidentally with the peak in proliferation and differentiation of vascular cells. It is highly expressed in adventitial vasa vasorum of injured arteries suggesting the involvement of T-cadherin in the processes of angiogenesis after vessel injury.

Takayasu's arteritis

aortic arch syndromeTakayasuTakayasu arteritis
The "pulseless phase" is characterized by vascular insufficiency from intimal narrowing of the vessels manifesting as arm or leg claudication, renal artery stenosis causing hypertension, and neurological manifestations due to decreased blood flow to the brain. Of note is the function of renal artery stenosis in the causation of high blood pressure: Normally perfused kidneys produce a proportionate amount of a substance called renin.

External support

In cardiac surgery and vascular surgery, external support (or external stent) is a type of scaffold made of metal or plastic material that is inserted over the outside of the vein graft in order to decrease the intermediate and late vein graft failure after bypass surgery (e.g. CABG). An external support (external stent) should be differentiated from a stent. An external support is placed on the outside of the vessel whereas a stent is inserted into the lumen of a vessel. Veins are adapted to an environment of low pressure and low flow.

Timeline of cardiovascular disease

This is a timeline of cardiovascular disease (CVD), focusing on scientific development and major worldwide organizations and events concerning CVD.

Angiopathy

damaged
In macroangiopathy, atherosclerosis and a resultant blood clot forms on the large blood vessels, sticks to the vessel walls, and blocks the flow of blood. Macroangiopathy may cause other complications, such as ischemic heart disease, stroke and peripheral vascular disease which contributes to the diabetic foot ulcers and the risk of amputation. In microangiopathy, the walls of the smaller blood vessels become so thick and weak that they bleed, leak protein, and slow the flow of blood through the body.

List of ICD-9 codes 390–459: diseases of the circulatory system

List of ICDdiseases of the circulatory system
Occlusion and stenosis of precerebral arteries. Occlusion and stenosis of basilar artery. Occlusion and stenosis of carotid artery. Occlusion and stenosis of vertebral artery. Occlusion of cerebral arteries. Cerebral thrombosis. Cerebral thrombosis without cerebral infarction. Cerebral thrombosis with cerebral infarction. Cerebral embolism. Cerebral embolism without cerebral infarction. Cerebral embolism with cerebral infarction. Transient cerebral ischemia. Basilar artery syndrome. Vertebral artery syndrome. Subclavian steal syndrome. Vertebrobasilar artery syndrome. Transient ischemic attack, unspec. Acute but ill-defined cerebrovascular disease.

List of MeSH codes (C14)

C14
. --- aortic valve stenosis. --- aortic stenosis, supravalvular. --- williams syndrome. --- aortic stenosis, subvalvular. --- cardiomyopathy, hypertrophic. --- discrete subaortic stenosis. --- heart murmurs. --- heart valve prolapse. --- aortic valve prolapse. --- mitral valve prolapse. --- tricuspid valve prolapse. --- mitral valve insufficiency. --- mitral valve stenosis. --- pulmonary atresia. --- pulmonary valve insufficiency. --- pulmonary valve stenosis. --- leopard syndrome. --- pulmonary subvalvular stenosis. --- tricuspid atresia. --- tricuspid valve insufficiency. --- tricuspid valve stenosis. --- coronary disease. --- angina pectoris. --- angina, unstable. --- angina pectoris, variant

Secondary hypertension

secondarysecondary high blood pressure
Kidney disease / renal artery stenosis – the normal physiological response to low blood pressure in the renal arteries is to increase cardiac output (CO) to maintain the pressure needed for glomerular filtration. Here, however, increased CO cannot solve the structural problems causing renal artery hypotension, with the result that CO remains chronically elevated. Renal segmental hypoplasia (Ask-Upmark kidney). Neurogenic hypertension – excessive secretion of norepinephrine and epinephrine which promotes vasoconstriction resulting from chronic high activity of the sympathoadrenal system, the sympathetic nervous system and the adrenal gland.

Aortic dissection

dissecting aortic aneurysmdissectionthoracic aortic dissection
Aortic dissection may be a late sequela of heart surgery. About 18% of individuals who present with an acute aortic dissection have a history of open-heart surgery. Individuals who have undergone aortic valve replacement for aortic insufficiency are at particularly high risk because aortic insufficiency causes increased blood flow in the ascending aorta. This can cause dilatation and weakening of the walls of the ascending aorta. Syphilis only potentially causes aortic dissection in its tertiary stage. As with all other arteries, the aorta is made up of three layers, the intima, the media, and the adventitia.

Atrial fibrillation

paroxysmal atrial fibrillationatrial fibrilationatrial arrhythmia
Cardiovascular factors known to be associated with the development of AF include high blood pressure, coronary artery disease, mitral valve stenosis (e.g., due to rheumatic heart disease or mitral valve prolapse), mitral regurgitation, left atrial enlargement, hypertrophic cardiomyopathy (HCM), pericarditis, congenital heart disease, and previous heart surgery. Additionally, lung diseases (such as pneumonia, lung cancer, pulmonary embolism, and sarcoidosis) are thought to play a role in certain people. Disorders of breathing during sleep such as obstructive sleep apnea (OSA) are also associated with AF. Obesity is a risk factor for AF.

Gaseous signaling molecules

gaseous signaling moleculegasotransmittergasotransmitters
Smooth muscle cell proliferation is one of important mechanisms of hypertensive remodeling of blood vessels and their stenosis, so it is an important pathogenetic mechanism in arterial hypertension and atherosclerosis. Endogenous sulfur dioxide in low concentrations causes endothelium-dependent vasodilation. In higher concentrations it causes endothelium-independent vasodilation and has a negative inotropic effect on cardiac output function, thus effectively lowering blood pressure and myocardial oxygen consumption. The vasodilating effects of sulfur dioxide are mediated via ATP-dependent calcium channels and L-type ("dihydropyridine") calcium channels.

Magnetic resonance angiography

magnetic resonance angiogramMRAmagnetic resonance
Magnetic resonance angiography is used to generate images of arteries (and less commonly veins) in order to evaluate them for stenosis (abnormal narrowing), occlusions, aneurysms (vessel wall dilatations, at risk of rupture) or other abnormalities. MRA is often used to evaluate the arteries of the neck and brain, the thoracic and abdominal aorta, the renal arteries, and the legs (the latter exam is often referred to as a "run-off"). A variety of techniques can be used to generate the pictures of blood vessels, both arteries and veins, based on flow effects or on contrast (inherent or pharmacologically generated).

Endothelial dysfunction

cell damage
Sirolimus eluting stents were previously used because they showed low rates of in-stent restenosis, but further investigation showed that they often impair endothelial function in humans and worsen conditions. One drug used to inhibit restenosis is iopromide-paclitaxel. Treatment of hypertension and hypercholesterolemia may improve endothelial function in people taking statins (HMGCoA-reductase inhibitor), and renin angiotensin system inhibitors, such as ACE inhibitors and angiotensin II receptor antagonists.

List of Autopsy: The Last Hours of... episodes

episodes
* Lists of people by cause of death * List of deaths from drug overdose and intoxication

Ankle–brachial pressure index

ankle brachial pressure indexankle-brachial indexABPI
Studies have shown the sensitivity of ABPI is 90% with a corresponding 98% specificity for detecting hemodynamically significant (Serious) stenosis >50% in major leg arteries, defined by angiogram. However, ABPI has known issues: When performed in an accredited diagnostic laboratory, the ABI is a fast, accurate, and painless exam, however these issues have rendered ABI unpopular in primary care offices and symptomatic patients are often referred to specialty clinics due to the perceived difficulties.

MTOR inhibitors

mTOR inhibitorability to inhibit mTORinhibitors
Since then, rapamycin has also shown to be effective for preventing coronary artery re-stenosis and for the treatment of neurodegenerative diseases. The development of rapamycin as an anticancer agent began again in the 1990s with the discovery of temsirolimus (CCI-779). This was a novel soluble rapamycin derivative that had a favorable toxicological profile in animals. More rapamycin derivatives with improved pharmacokinetics and reduced immunosuppressive effects have since then been developed for the treatment of cancer. These rapalogs include temsirolimus (CCI-779), everolimus (RAD001), and ridaforolimus (AP-23573) which are being evaluated in cancer clinical trials.

CYR61

Cysteine-rich angiogenic inducer 61
CYR61 is overexpressed in vascular smooth muscle cells of atherosclerotic lesions and in the neointima of restenosis after balloon angioplasty, both in rodent models and in humans. Suppression of CYR61 expression results in reduced neointimal hyperplasia after balloon angioplasty, an effect that is reversed by delivery of CYR61 via gene transfer In a mouse model of oxygen-induced retinopathy, expression of CYR61 in the vitreous humor produced significant beneficial effects in repairing damaged vasculature. Angiogenesis is essential for the supply of oxygen and nutrients to nourish the growing tumor.

Ostial disease

Ostial disease, namely coronary ostial stenosis, is the occlusion of coronary ostium. Causing factors include atherosclerosis, syphilis, Kawasaki disease, and Takayasu's arteritis, etc.

Protease-activated receptor

PAR proteinsPAR1
PARs contribute to the pro-inflammatory response observed in atherosclerosis and restenosis. Recent research has also implicated these novel receptors in muscle growth and bone cell differentiation and proliferation. In T cells, activation of PAR1, PAR2 and PAR3 induce tyrosine phosphorylation of VAV1. Activation of PARs also led to an increase in tyrosine phosphorylation of ZAP-70 and SLP-76, two key proteins in T cell receptor (TCR) signalling.

Vertebral artery dissection

cervical artery dissectionDissection of the vertebral arteryvertebral
Atherosclerosis does not appear to increase the risk. There have been numerous reports of associated risk factors for vertebral artery dissection; many of these reports suffer from methodological weaknesses, such as selection bias. Elevated homocysteine levels, often due to mutations in the MTHFR gene, appear to increase the risk of vertebral artery dissection. People with an aneurysm of the aortic root and people with a history of migraine may be predisposed to vertebral artery dissection.

ICD-10 Chapter IX: Diseases of the circulatory system

Chapter IXDiseases of the circulatory system
Occlusion and stenosis of other precerebral artery. Occlusion and stenosis of unspecified precerebral artery. Occlusion and stenosis of cerebral arteries, not resulting in cerebral infarction. Occlusion and stenosis of middle cerebral artery. Occlusion and stenosis of anterior cerebral artery. Occlusion and stenosis of posterior cerebral artery. Occlusion and stenosis of cerebellar arteries. Occlusion and stenosis of multiple and bilateral cerebral arteries. Occlusion and stenosis of other cerebral artery. Occlusion and stenosis of unspecified cerebral artery. Other cerebrovascular diseases. Cerebral aneurysm, nonruptured. Cerebral atherosclerosis. Progressive vascular leukoencephalopathy.

Collateralization

collateral blood vessels
Atherosclerosis. Axonal collateralization and its dependence on Dendritic arborization.