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)

Chronic hypertension increases the risk of myocardial infarction and the morbidity and mortality associated with it. Although accelerated atherosclerosis is partially responsible, other abnormalities in the coronary circulation associated with hypertension, such as decreased coronary vascular capacity and capillary density, could also contribute. To evaluate the effects of these nonatherosclerotic abnormalities, we produced sudden coronary occlusion in nine chronically hypertensive dogs. The mean aortic pressure and left ventricular mass were about 50% greater in hypertensive dogs than in the nine controls. Before occlusion and 5 min and 49 h after occlusion, myocardial blood flow was measured with tracer microspheres. Also, the extent of infarction in selected myocardial segments was quantified histologically. We found that coronary occlusion reduced flows to a similar extent, and that, over a 48-h period, collateral flow increased to a similar extent in the two groups. In addition, the amount of necrosis associated with a given degree of ischemia was similar in the two groups. Although the extent of the left ventricle that became ischemic was greater in the hypertensive dogs (28 +/- 2 vs. 18 +/- 4%; P < 0.05), chronic hypertension and left ventricular hypertrophy did not limit the recruitment of collateral supply or increase the amount of necrosis associated with a given degree of ischemia.
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PMID:Myocardial infarction in dogs with chronic hypertension and left ventricular hypertrophy. 644 77

A 41-year-old man developed persistent angina pectoris following blunt trauma to his chest. Three months after the injury coronary angiography demonstrated 80% obstruction of the mid-left anterior descending coronary artery. There was no evidence of atherosclerosis in the remaining coronary arteries. Therefore the assumption is made that blunt trauma can induce incomplete coronary occlusion resulting in classic angina pectoris in apparently otherwise normal coronary arteries. The suggested mechanism of injury to the coronary vessel is either intimal tear and/or subintimal hemorrhage with incomplete luminal thrombosis.
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PMID:Coronary artery obstruction due to blunt chest trauma with residual angina pectoris. 688 2

Four patients with chronic systemic lupus erythematosus (SLE) in whom myocardial infarction occurred at an unusually early age are described. The evidence suggests that the coronary occlusion was due to atherosclerosis. There was no evidence that active arteritis played any role. The only risk factor for atherosclerotic disease was hypertension. All patients had had both central nervous system and renal disease and had been taking corticosteroids for a minimum of 9 years. It is suggested that hypertension aggravated by chronic corticosteroid administration may be an important risk factor for atherosclerosis in patients with SLE.
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PMID:Myocardial infarction in four young patients with SLE. 688 70

With the arteriographic demonstration of coronary arterial spasm, fundamental questions have been raised concerning the role of spasm in myocardial ischemia and infarction. It is now clear that coronary arterial spasm is the cause of Prinzmetal's variant angina pectoris in patients with and without coronary atherosclerosis. In most patients with coronary heart disease, major ischemic events frequently result from increased myocardial oxygen demand or coronary thrombosis. However, recent evidence suggests that coronary arterial spasm may initiate or contribute to the development of unstable angina pectoris, acute myocardial infarction, and sudden death in these patients. Thus, episodes of myocardial ischemia and infarction are induced by factors, acting singly or in combination, that augment myocardial oxygen demand or diminish myocardial oxygen supply, and the latter alteration can result from thrombotic coronary occlusion or a dynamic increase in coronary arterial tone (that is, coronary arterial spasm).
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PMID:The role of coronary arterial spasm in ischemic heart disease. 689 63

The formation of platelet aggregates has been suggested to be the initial step in coronary occlusion and the subsequent myocardial infarction (AMI). By scanning electron microscopy we followed: the platelet morphology and aggregation, the macrophage (M) morphology and the lymphocyte (T, B) count and structure in 11 patients with AMI and in 18 patients with unstable angina (UA). Generally, in the patients with AMI, most of the platelets presented relatively frequent (42.5%) or very frequent pseudopodia (35.27%) and the network of surface extensions was associated with several huge platelet aggregates in 6 patients. The mean lymphocyte count was: T = 40.36 +/- 23.95%; B = 28.09 +/- 7.38%; M = 31.54 +/- 21.25%. In the patients with unstable angina the proportion of platelets with pseudopodia was more reduced, namely, that of platelets with relatively frequent pseudopodia was 33.8% and with very frequent pseudopodia was 27.8%. The mean lymphocyte count was: T = 40.30 +/- 20.24%; B = 34.6 +/- 14.39%; M = 25 +/- 10.50%. These data indicate that platelet changes and the formation of aggregates can be an important factor in the occurrence of AMI. The change of immunocompetent cell count in both groups of coronary patients suggests the association of an immunologic process in coronary atherosclerosis.
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PMID:Changes of human platelets studied by scanning electron microscopy in acute myocardial infarction. 698 94

The effects of smoking and alcohol intake on the extent of coronary artery occlusion were studied in 2989 men undergoing a diagnostic coronary arteriography. Smoking showed an exposure-related enhancing effect on the extent of coronary artery occlusion. Conversely, alcohol consumption demonstrated an attenuating dose-related effect, offsetting the increased coronary occlusion associated with smoking. Alcohol intake should be considered in studies evaluating the risk factors--coronary artery disease interaction.
Atherosclerosis 1982 Jun
PMID:Smoking, alcohol and coronary artery occlusion. 711 64

Previous reports have described an inverse relationship between alcohol consumption and the prevalence of myocardial infarction or the extent of coronary artery occlusion. The study reported here explored the relationship between patterns of alcohol intake and coronary occlusion in 526 patients who have had coronary arteriography. Patients were characterized as regular drinkers, occasional drinkers and non-drinkers. Regular drinkers were further characterized as drinking relatively consistent amounts or variable amounts. The inverse correlation between amounts of alcohol consumed and coronary occlusion found in previous studies was reaffirmed. It was also observed that the pattern of alcohol intake was related to the degree of occlusion. Higher levels of occlusion were found among non-drinkers, occasional drinkers, and regular drinkers with patterns of variable intake, while significantly lower levels of occlusion were observed for regular drinkers who drank relatively consistent amounts (P = 0.014). Furthermore, while occlusion scores were inversely correlated with amounts consumed by regular drinkers with consistent intake (P = 0.019), drinkers with variable drinking patterns had higher occlusion scores regardless of amounts consumed. Analyses of serum lipids according to drinking patterns showed a significant association between the total/HDL cholesterol ratio and drinking patterns. These findings suggest that whatever attenuating effect alcohol consumption might exert on coronary occlusion, it appears to be reversed by a variable or sporadic pattern of alcohol intake.
Atherosclerosis 1982 Jun
PMID:Effects of drinking patterns on the relationship between alcohol an coronary occlusion. 711 68

The effects of experimental coronary atherosclerosis on myocardial high energy phosphates and regional coronary perfusion and oxygen delivery were studied. Hypercholesterolemic (HC) New Zealand white rabbits developed mild to moderate coronary vascular disease in 4 months when serum cholesterol levels were maintained at 1500--2000 mg/dl. Resting left ventricular levels of creatine phosphate, adenosine triphosphate (ATP), and the cellular energy charge were unaltered after 2 months of diet but were decreased after 4 and 6 months. Tissue lactate and the lactate/pyruvate ratio were increased after 4 months, suggesting mild tissue ischemia. The regional blood flow rate was measured in rabbits given pentobarbital after 6 months of diet using labeled microspheres, and the response to stress was tested after 5 minutes of hypoxic ventilation (5% O2/N2). The percentage of cardiac output to subendocardium (endo) and subepicardium (epi) in HC rabbits and that in control animals were similar at rest, but unlike that of control animals, the endo perfusion did not increase significantly in HC animals during hypoxic stress. Baseline regional left ventricular oxygen deliveries were similar between groups, but the baseline endo/epi oxygen delivery ratio was reduced in HC rabbits. In control rabbits hypoxia did not alter total O2 delivery, and the endo/epi oxygen delivery ratio was constant, whereas hypoxia in HC animals produced a decrease in total oxygen delivery and a further decrease in the endo/epi oxygen delivery ratio. Thus, moderate long-term coronary occlusive disease produced alterations in the distribution of coronary perfusion that are similar to those after acute partial occlusion, ie, selective reductions in blood flow and oxygen delivery to subendocardium. These results may relate to the pathogenesis of subendocardial infarction in man, which often occurs in the absence of complete coronary occlusion.
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PMID:Regional coronary perfusion and bioenergetics in experimental atherosclerosis. 736 55

Until a few years ago coronary atherosclerosis was thought to be a slowly progressive disease eventually leading to total coronary occlusion and myocardial infarction. Recent angiographic studies have shown, instead, that mild or moderate coronary stenoses have the highest risk of causing acute coronary syndromes when complicated by thrombus formation which, in turn, appears to be due to a complex interaction between the atherosclerotic background and acute ischemic stimuli. The tendency of the atherosclerotic background to develop thrombosis may be different in different patients, as indicated by the observation that the risk factor profile of patients who present with chronic coronary syndromes is different from that of patients who present with acute syndromes. The acute ischemic stimuli so far identified are: a sudden local thrombogenic stimulus; a transient systemic increase in systemic pro-coagulant activity; a transient increase in proximal and/or distal coronary tone. The recent observation of inflammatory cells activation, including T-lymphocytes, in patients with acute ischemic syndromes raises the intriguing possibility that a specific antigenic stimulus may play an important pathogenetic role.
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PMID:[Interactions between atherosclerosis and ischemic stimuli in the pathogenesis of acute coronary syndromes]. 763 63

Several experimental trials are under way to correct the deficiency of LDL receptor function known as Familial Hypercholesterolemia (FH) that develops devastating atherosclerosis leading to premature fatal coronary occlusion. Recently, a 28-year-old FH homozygous woman has received ex vivo autologous liver transplantation after transduction with retroviral vector expressing functional LDL receptors. The outcome is partially successful but is still controversial because of an argument that the apparent small decrease in the total plasma cholesterol level is not necessarily caused by the correction of the LDL receptor expression. In addition to retrovirus, adenovirus vector and non-viral methods are being employed as potential tools for FH gene therapy.
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PMID:[Perspective of gene therapy in hyperlipoproteinemia]. 785 27


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