Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A morphologic study of 376 hearts from individuals who died between 75 and 98 years of age demonstrated senile amyloidosis of the heart in 307 (82%) of the cases, using the Congo red stains for polarized light studies and the thiosine red for luminescent microscopy. The frequency of cardiac amyloidosis detection increased with age, and reached 100% in those above 90. Clinico-anatomical correlations showed repolarization changes to be the most common findings (80%), followed by arrhythmia (over 50%), conductivity disorders and reduced voltage of electrocardiographic waves. Chronic heart failure was less common (about 10%). In most cases, moderately marked coronary atherosclerosis was also found at autopsy. Amyloidosis was thought to be making a more significant contribution towards myocardial lesions, as compared to atherosclerosis, in elderly people above 85 years of age.
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PMID:[Senile amyloidosis of the heart]. 370 92

Nitric oxide (NO), derived from the vascular endothelium and other cells of the cardiovascular system, has important roles in physiological regulation of blood flow and may have pathophysiological functions in cardiovascular disease. The mechanisms involved in NO-induced vasodilatation and cytotoxicity are briefly reviewed in the context of inflammatory reactions and cardiovascular function. Although NO can hyperpolarize vascular smooth muscle, activation of the endothelium can induce hyperpolarization and vasodilatation by other means. Endogenous inhibitors of NO generated by leucocytes may compromise blood flow distribution after ischaemia and reperfusion injury. Chronic heart failure is associated simultaneously with impairment of endothelium-dependent vasodilatation and with excess production of NO via the inducible NO synthase (iNOS), although it is unclear whether the latter ameliorates or exacerbates ventricular dysfunction. Excess NO production is also one of the earliest signs of transplant rejection, and suppression of iNOS expression by immunosuppressant drugs such as cyclosporin A might be one means by which these drugs protect allografts. Disturbances in the activity of NOS isoforms in the artery wall also accompany the development of atherosclerosis, providing conditions propitious for vasospasm and thrombosis. Reversing the NO defects with therapeutic agents, including angiotensin converting enzyme (ACE) inhibitors, offers promise in protecting against some manifestations of vascular disease.
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PMID:Endogenous nitric oxide in cardiovascular disease and transplantation. 754 30

Nitric oxide (NO), derived from the vascular endothelium or other cells of the cardiovascular system, has an important role in physiological regulation of blood flow and has pathophysiological functions in cardiovascular disease. The mechanisms and enzymes involved in the biosynthesis of NO and biological actions of NO, including vasodilatation, cytotoxicity and inflammation, are briefly reviewed. These reactions involving NO cause pathological disturbances of arterial function, coronary blood flow regulation, and may contribute to cardiac myocyte dysfunction. NO and prostacyclin (PGI2), which is also released from the endothelium, act synergistically to inhibit platelet aggregation and adhesion, and in some arteries these mediators also synergise in terms of vasodilatation. In addition, NO is capable of hyperpolarizing vascular smooth muscle, but activation of the endothelium may cause hyperpolarization and may thus promote vasodilatation by an additional mechanism. After myocardial ischemia and reperfusion, production of NO and superoxide radicals represent important mechanisms of cytotoxicity, causing injury to the coronary endothelium and myocytes and compromising ventricular contractile function. Moreover, upon reperfusion endothelium-dependent vasodilatation is impaired and the coronary arteries constrict, leading to irregular myocardial perfusion. This is a consequence of the accumulation of activated leucocytes that we found to generate endogenous inhibitors of NO. These factors have yet to be fully characterised, but clearly they may have a role in irregularities of myocardial reperfusion and cellular injury. Chronic heart failure is associated both with impairment of endothelium-dependent vasodilatation and with excess production of NO via the inducible NO synthase (iNOS), although it is unclear whether the latter assists or compromises ventricular contractile performance under these conditions. Disturbances in the activity of isoforms of NO synthase in the artery wall also accompany the development of atherosclerosis, providing conditions propitious for vasospasm and thrombosis, and perhaps contributing to cell proliferation. Reversing these NO defects with therapeutic agents including angiotensin converting enzyme (ACE) inhibitors offers promise in protecting against some manifestations of vascular disease.
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PMID:Nitric oxide in coronary artery disease: roles in atherosclerosis, myocardial reperfusion and heart failure. 880 87

Chronic heart failure (CHF) remains widespread and prognostically unfavorable complication of various cardiovascular diseases. Most patients with CHF have atherosclerosis of coronary arteries. Main method of treatment of this condition is endovascular revascularization. In this study we conducted detailed analysis of effects of transluminal balloon coronary angioplasty (TBCA) with stenting on clinical-functional status, changes of perfusion and contractility of left ventricular myocardium in patients with CHF of ischemic etiology. We also identified factors producing unfavorable impact on restoration of myocardial perfusion after stenting.
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PMID:[Effects of coronary angioplasty on clinical status, perfusion myocardial contractility in patients with ischemic chronic heart failure]. 2517 82