Atherosclerosis Myocardial infarct

However, most pathological conditions, believed to involve derangements in the thromboxane biosynthesis - or in the thromboxane/prostacyclin balance - concern the cardiovascular system. A large number of diseases affecting this organ system have been studied in this respect, i.e. atherosclerosis, myocardial infarction, coronary artery disease with angina of various etiologies, thrombotic disorders, hemostatic defects, circulatory shock, ulcerative diseases, and so on. The possible roles of thromboxane and prostacyclin in the cardiovascular system have been discussed in several reviews, e.g. refs. 32, 33, 348-354. 

Production of advanced coronary atherosclerosis, myocardial infarction and sudden death" in swine. 

Lee KT, Jarmolych J, Kim DN (1971) Production of advanced coronary atherosclerosis, myocardial infarction, and sudden death in swine. Exp Mol Pathol 15 170-190... 

Other Cardiovascular Agents Effecting Atherosclerosis. A large amount of clinical data is available concerning semm Upid profiles in patients subjected to dmg therapy for other cardiovascular diseases. Atheroma, for example, may be the underlying cause of hypertension and myocardial infarction. There are on the order of 1.5 million heart attacks pet year in the United States (155). 

Thrombolytic Enzymes. Although atherosclerosis and the accompanying vascular wall defects are ultimately responsible for such diseases as acute pulmonary embolism, arterial occlusion, and myocardial infarction, the lack of blood flow caused by a fibrin clot directly results in tissue injury and in the clinical symptoms of these devastating diseases (54). Thrombolytic enzyme therapy removes the fibrin clot by dissolution, and has shown promise in the treatment of a number of thrombo-occlusive diseases (60). 

Carotenoids and cardiovascular diseases — Numerous epidemiological studies aimed to study the relationship of carotenoids and cardiovascular diseases (CVDs) including coronary accident risk and stroke. It appeared then that observational studies, namely prospective and case-control studies, pointed to a protective effect of carotenoids on myocardial infarct and stroke, but also on some atherosclerosis markers such as intima media thickness (IMT) of the common carotid artery (CCA) and atheromatous plaque formation. 

Some prospective and case-control studies also investigated the relationship of carotenoids and the evolution of CCA-IMT. Although the EVA study showed no association between total carotenoids and IMT, others like the ARIC study, the Los Angeles Atherosclerosis Study, " and the Kuopio Ischaemic Heart Disease Risk Factor Study demonstrated the protective role of isolated carotenoids such as lycopene, lutein, zeaxanthin, and P-cryptoxanthin on IMT. Thus, findings from prospective and case-control studies have suggested that some carotenoids such as lycopene and P-carotene may present protective effects against CVD and particularly myocardial infarcts and intima media thickness, a marker of atherosclerosis. 

O Ischemic heart disease results from an imbalance between myocardial oxygen demand and oxygen supply that is most often due to coronary atherosclerosis. Common clinical manifestations of ischemic heart disease include chronic stable angina and the acute coronary syndromes of unstable angina, non-ST-segment elevation myocardial infarction, and ST-segment elevation myocardial infarction. 

Hypertension is the most common cardiovascular disease in fact, nearly 25% of adults in the U.S. are considered hypertensive. Hypertension is defined as a consistent elevation in blood pressure such that systolic/diastolic pressures are >140/90 mmHg. Over time, chronic hypertension can cause pathological changes in the vasculature and in the heart. As a result, hypertensive patients are at increased risk for atherosclerosis, aneurysm, stroke, myocardial infarction, heart failure, and kidney failure. There are several categories of antihypertensive agents ... 

Various antibody preparations have been developed that facilitate imaging of vascular-related conditions, including myocardial infarction, deep vein thrombosis and atherosclerosis. Anti-myosin monoclonal antibody fragments (Fab) labelled with mIn, for example, have been used for imaging purposes in conjunction with a planar gamma camera. The antibody displays specificity for intracellular cardiac myosin, which is exposed only upon death of heart muscle tissue induced by a myocardial infarction (heart attack). 

The response-to-injury hypothesis states that risk factors such as oxidized LDL, mechanical injury to the endothelium, excessive homocysteine, immunologic attack, or infection-induced changes in endothelial and intimal function lead to endothelial dysfunction and a series of cellular interactions that culminate in atherosclerosis. The eventual clinical outcomes may include angina, myocardial infarction, arrhythmias, stroke, peripheral arterial disease, abdominal aortic aneurysm, and sudden death. 

K6. Kark, J. D., Sandholzer, C., Friedlander, Y., and Utermann, G., Plasma Lp(a), apolipopro-tein(a) isoforms and acute myocardial infarction in men and women A case-control study in the Jerusalem population. Atherosclerosis (Shannon, Irel.) 98, 139-151 (1993). 

M22. MBewu, A. D., Durrington, P. N., Bullied, S., and Mackness, M. I., The immediate effect of streptokinase on serum lipoprotein(a) concentration and the effect of myocardial infarction on serum lipoprotein(a), apolipoprotein A1 and B. lipids and C-reactive protein. Atherosclerosis (Shannon, Irel.) 103, 65-71 (1993). 

Many studies have shown that ginseng has a protective effect on the development of atherosclerosis that may lead to myocardial infarction and other cardiovascular diseases. The preventive effects on cardiovascular diseases of ginseng include its potential antihypertensive and antiatherosclerotic effects. Ginsenosides are likely to be responsible for some of these effects as they have been shown to have inhibitory effects on platelet aggregation and to suppress thrombin formation as well as an effect on blood vessel contraction. 

Aging (skin and other tissues), myocardial infarct or stroke, inflammation, rheumatoid arthritis, atherosclerosis, pulmonary disorders (asthma and chronic obstructive pulmonary diseases), radiation injury, organ transplant rejection, psoriasis, hypertension, AIDS, multiple types of cancer, neuro-degenerative diseases (Parkinson s), diabetes, muscular dystrophy... 

Accumulation of homocystine in blood is associated with cardiovascular disease deep vein thrombosis, thromboembolism, and stroke dislocation of the lens (ectopic lens) and mental retardation. Homocystinemia caused by an enzyme deficiency is a rare, but severe, condition in which atherosclerosis in childhood is a prominent finding. These children often have myocardial infarctions before 20 years of age. Ail patients excrete high levels of homocystine in the urine. Treatment includes a diet low in methionine. The two major enzyme deficiencies producing homocystinemia are ... 

Accelerated atherosclerosis and increased risk of myocardial infarction... 

The ACE gene encodes two isozymes (somatic ACE isozyme and germinal ACE isozyme). ACE is a membrane-bound enzyme on the surface of vascular endothelial cells that also circulates in plasma and shows great individual variability determined by an I/D polymorphism in intron 16 of the ACE gene (ACE-I/D polymorphism). More than 160 ACE polymorphisms have been reported, 34 of which are located in coding regions, and 18 are missense mutations (606). ACE-related polymorphic variants have been associated with hypertension, atherosclerosis, stroke, left ventricular hypertrophy, chronic renal failure in IgA nephropathy, Henoch-Schonlein purpura nephritis, mechanical efficiency of skeletal muscle, intracranial aneurysms, susceptibility to myocardial infarction, diabetic nephropathy, AD, and longevity (12,606,607). 

Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone.

Coronary atherosclerosis angina pectoris, myocardial infarction, arrhythmia Atherosclerosis of cerebral vessels cerebral infarction stroke... 

Arterial thrombi (white thrombi) are formed initially from both platelets and fibrin in medium-sized arteries on the basis of atherosclerosis. These thrombi can lead to symptoms of, among others, myocardial ischemia and myocardial infarction. The treatment is primarily aimed at prevention of thrombus formation with platelet aggregation inhibitors. For the treatment of myocardial infarction thrombolytic agents are used and for secondary prevention both oral anticoagulants and anti-platelet drugs are employed. 

ACE inhibitors are widely prescribed for patients with atherosclerosis, hypertension, or diabetes, and after myocardial infarction, because of proven beneficial effects in each of these groups. In light of the results in the setting of stent restenosis, whether a patient with hypertension or some other target disorder who carries the DD genotype derives less benefit from ACE inhibitor therapy warrants consideration. 

Increased production of ET-1 has been implicated in a variety of cardiovascular diseases, including hypertension, cardiac hypertrophy, heart failure, atherosclerosis, coronary artery disease, and myocardial infarction. ET-1 also participates in pulmonary diseases, including asthma and pulmonary hypertension, as well as in several renal diseases. 

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