Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of cerebrovascular lesions is affected by race. Blacks and Japanese have more intracranial occlusive cerebrovascular disease, while whites have more extracranial disease. Despite a high incidence of stroke in China, there are few formal studies of the distribution of vascular occlusive disease in Chinese populations. We compared clinical and angiographic features of 24 white and 24 Chinese patients with symptomatic occlusive cerebrovascular disease. In symptomatic vascular territories, whites had more severe (greater than or equal to 50% stenosis) extracranial lesions, while Chinese had more severe intracranial lesions. When we counted mild and severe lesions in a symptomatic territory, whites had more extracranial lesions while Chinese had more intracranial lesions. When we combined symptomatic and asymptomatic territories, whites had more extracranial lesions, while Chinese had more intracranial lesions. White patients reported more transient ischemic attacks. The distribution of lesions, however, was not explained by differences in incidence of transient ischemia, hypertension, diabetes, hypercholesterolemia, or ischemic heart disease between the groups. The preponderance of intracranial vascular lesions in Chinese patients is similar to that seen in blacks and Japanese. Racial differences in the occurrence of extracranial and intracranial lesions raise the possibility of a different underlying pathophysiology for the 2 locations.
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PMID:Chinese-white differences in the distribution of occlusive cerebrovascular disease. 221 45

We define the concept of reperfusion injury, and we present a background chronology of experimental work supporting and questioning this concept. We identify several new influences, such as current clinical interest in thrombolytic therapy for acute ischemia of heart and brain and the growing recognition of endothelium as a regulator of homeostasis. We propose that these influences will encourage a reexamination of reperfusion injury as a factor in the ultimate outcome of tissue exposed to reversible ischemia. We briefly discuss the major mechanisms presently implicated in reperfusion injury--loss of calcium homeostasis, free radical generation, leukocyte-mediated injury, and acute hypercholesterolemia.
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PMID:Background review and current concepts of reperfusion injury. 224 24

Sudden fissuring of an atherosclerotic plaque has been suggested as the primary trigger of transient spontaneous ischemia in both the coronary and cerebral circulation. Measurements of urinary 11-dehydro-TXB2 and 2,3-dinor-TXB2, as well as results of Aspirin trials, have suggested that episodic platelet activation at the site of this acute vascular lesion is mediated, at least partly, by enhanced thromboxane (TX) A2 biosynthesis. Thus, episodic increases in metabolite excretion have been detected in unstable angina. Aspirin (75-325 mg/day) prevents about one third of all fatal and nonfatal thrombotic events in this setting. That a similar "dynamic" thrombotic process occurs during the early phase of acute myocardial infarction is suggested by thromboxane metabolite measurements and by the results of the ISIS-2 trial showing a similar impact of short-term Aspirin therapy to that seen in unstable angina. Percutaneous transluminal coronary angioplasty is associated with transiently enhanced TXA2 biosynthesis and Aspirin-suppressable periprocedural thrombotic complications. On the other hand, both non-insulin-dependent diabetes mellitus and type IIa hypercholesterolemia are associated with a relatively reproducible and persisting abnormality of TXA2-dependent platelet function. This association is likely to reflect a systemic rather than localized stimulus to platelet activation and a continuous rather than episodic alteration. Low-dose (50 mg/day) Aspirin can largely suppress thromboxane metabolite excretion in both diseases. Thus, low-dose Aspirin and/or selective prostaglandin H2/TXA2-receptor antagonists may be important tools to test the hypothesis that TXA2-dependent platelet activation represents an important transducer of the enhanced thrombotic risk associated with these metabolic abnormalities.
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PMID:Thromboxane biosynthesis in cardiovascular diseases. 226 Jan 37

We prospectively examined the prognostic significance of silent myocardial ischemia detected by ambulatory electrocardiogram (ECG) monitoring during daily life in 107 patients with long-term stable angina who were symptomatically controlled on conventional antianginal agents. Forty-six patients (group 1) demonstrated one or more episodes (87% silent) of myocardial ischemia; the remaining 61 patients (group 2) had no ischemic ST segment changes. During the mean follow-up period of 23 +/- 8 months, 11 cardiac deaths (five sudden and six nonsudden) occurred in group 1, and five cardiac deaths (all nonsudden) occurred in group 2. Kaplan-Meier survival analysis between the groups confirmed that patients with silent ischemia (group 1) had worse prognoses during the follow-up period (p = 0.023). Although the higher incidence of hypertension, smoking, hypercholesterolemia, and diabetes in our patients might reflect a more sickly population of stable angina patients, the multivariate Cox's hazard function analysis of these and other variables including Q waves on ECG, exercise parameters, and ambulatory ECG findings revealed presence of silent ischemia during daily life as the most powerful and independent predictor of cardiac mortality (p = 0.01). These data indicate that, in such patients with stable angina, silent myocardial ischemia occurs frequently during treatment with conventional antianginal drugs and identifies a subset of patients who are at high risk of cardiac death.
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PMID:Silent ischemia during daily life is an independent predictor of mortality in stable angina. 230 19

We retrospectively studied the arteriograms of 135 men admitted for evaluation of lower extremity ischemia to examine whether race influences the severity of infragenicular occlusive disease. The scoring system prepared by the Ad Hoc Committee on Reporting Standards for the Society for Vascular Surgery and the International Society for Cardiovascular Surgery was used to grade the severity of stenosis in each of the upper, middle, and lower thirds of the anterior and posterior tibial and peroneal arteries (collectively called "infragenicular" arteries). The patients were divided into two groups: 83 blacks (140 arteriogram limbs) and 52 whites (87 arteriogram limbs). Disease severity scores between the groups were compared, and the existence of five known risk factors for atherosclerosis were considered for poststratification adjustment. Results showed that higher disease scores, indicating more severe disease, were found in the black population in every segment of the infragenicular arteries. The mean (+/- SE) score for all the infragenicular segments in blacks was significantly higher than that in the whites (2.08 +/- 0.05 vs 1.57 +/- 0.06, p less than 0.001). The black and white groups were comparable in terms of age (65.2 vs 64.6 years), prevalence of diabetes (20% vs 25%), smoking history (93% vs 90%), and hypercholesterolemia (51% vs 63%). Hypertension was more prevalent among the black patients (51% vs 27%, p less than 0.001). When only the non-hypertensive patients in both groups were considered, however; the mean severity score was still significantly higher in blacks (2.10 +/- 0.06 vs 1.42 +/- 0.06, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Race as a risk factor in the severity of infragenicular occlusive disease: study of an urban hospital patient population. 232 14

This retrospective study compared the results of percutaneous transluminal angioplasty (PTA) with those of infrainguinal bypass procedures in patients with critical arterial ischemia to determine which procedure had superior patency, limb salvage, and durability. The records of 54 patients who underwent 54 PTAs and 56 patients who underwent 63 infrainguinal bypasses (29 femoropopliteal and 34 femorodistal) from 1981 to 1987 were reviewed. In each patient PTA or bypass was the initial vascular procedure. Patients in both groups were comparable with respect to age, sex, and the presence of diabetes, hypertension, obesity, hypercholesterolemia, and smoking. Mean follow-up was 40 months (4 to 88 months) for the PTA group and 28 months (6 to 78 months) for the surgery group. Thirty-nine of the 54 patients (72%) were initially improved after PTA, whereas 15 patients (28%) showed no improvement. During follow-up, 20 initially successful PTAs reoccluded. Thirty-two of 54 patients (59%) underwent subsequent procedures, which included repeat PTA (10) and distal bypass (14). Patency determined by noninvasive Doppler studies was 18% at 2 years. Limb salvage, which included such secondary procedures, was 78%. Two-year patency for femoropopliteal bypasses was 68% with a limb salvage of 90%. Femorodistal bypasses had a 2-year patency of 47% and a limb salvage of 74%. No perioperative deaths occurred. Twenty-one of the 63 patients (33%) had subsequent procedures, which included thrombectomy (5) and bypass revision (9). In patients treated for limb-threatening ischemia the 2-year patency after femoropopliteal bypass (68%) or femorodistal bypass (47%) is significantly better than that from PTA (18%, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Percutaneous transluminal angioplasty versus surgery for limb-threatening ischemia. 213 83

Dynamics of changes in the myocardium of rabbits subjected to food hypercholesterolemia lasting from 6 to 16 weeks was investigated. An intensification of coronary atheromatosis was proportional to the duration of the high-cholesterol diet. There were observed focal and growing in time damages of cardiomyocytes. They were sharply outlined in atherosclerotically changed coronary arteries. The following morphological and histochemical changes have been observed: increased acidophilia and fuchsinophilia in the single and grouped muscle fibres, foci of infiltrations by mononuclear cells, contraction bands, and outlines of myocardial fibres, separation of myofibrils, granular disintegration of cardiomyocytes, healed infarcts, depletion and excessive accumulation of glycogen in muscle fibres, presence of neutral fats, cholesterol and its esters in atheromatous plaques of coronary arteries, presence of neutral fats in some cardiomyocytes: focal acid phosphates, loss of activity of Mg- and Ca-dependent ATPases and SDH: oedema of mitochondria with disorganization of cristae, disorganisation of fibres and lysis of myofilaments, margination of chromatin in cardiomyocyte nuclei, increased number of lysosomes, intensified symptoms of egzocytosis, widening of channels of sarcoplasmatic reticulum, oedema of endothelium of capillary vessels and increased number of the collagenous fibres in the interstitial space. The results of histological, histochemical and microscopic-electron investigations correlated with each other. It may be considered that the observed damages of cardiomyocytes precede myocardial infarction and result from progressive and increasing ischemia, hypoxia and accumulation of fat substances and cholesterol and its esters in intima of coronary arterioles as well as in cardiomyocytes.
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PMID:[Dynamics of lesions to the myocardium in experimental hyper- cholesterolemia]. 281 56

Hypercholesterolemia was induced in New Zealand white rabbits by feeding them a 0.5% cholesterol-enriched rabbit chow for 2 wk. Half of the cholesterol-fed rabbits were given lovastatin, a potent inhibitor of hydroxymethylglutaryl-coenzyme A reductase (HMG-CoA reductase), the rate limiting enzyme in cholesterol biosynthesis, and the other half were given its vehicle (i.e., DMSO). At the end of 2 wk, the rabbits underwent experimental myocardial ischemia or a sham ischemia procedure. Ischemic animals fed the cholesterol-enriched diet for 2 wk experienced much greater cardiac damage than ischemic rabbits fed the control diet, despite the absence of any atherosclerosis. Lovastatin was shown to protect the ischemic rabbit myocardium by three different indices of ischemic damage: (a) maintenance of creatine kinase (CK) activity in the ischemic myocardium; (b) reduced loss of free amino-nitrogen containing compounds from the ischemic myocardium; and (c) blunting the rise of plasma CK activity. These effects were not due to differences in myocardial oxygen demand between the groups. Arteries isolated from animals fed the cholesterol-enriched diet developed defects in endothelium-dependent relaxation in both large vessels as well as coronary resistance vessels. Acute hypercholesterolemia increases the severity of myocardial ischemia while at the same time impairing endothelium-dependent relaxation. These deleterious changes can be significantly attenuated by treatment with lovastatin.
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PMID:Cardiovascular effects of acute hypercholesterolemia in rabbits. Reversal with lovastatin treatment. 291 50

The cardiac prognosis of hypertensive patients has been able to be precisely determined over the last 20 years as a result of large-scale epidemiologic surveys. The incidence of ischemic heart disease and the importance of left ventricular hypertrophy have been clearly defined in the literature. In contrast, the incidence of sudden death and ventricular arrhythmias has been poorly taken into account, although hypertension increases the risk of sudden death to the same degree as coronary artery disease. The relative risk increases progressively as a function of the quintiles of distribution of blood pressure, reaching a value of 3.2 for the highest quintile. There is also a significant correlation between hypertension and ventricular arrhythmias. Hypertensive subjects with other cardiovascular risk factors such as hypercholesterolemia or smoking and with ventricular extrasystoles, reflecting the presence of silent ischemia, can be considered to be at high risk of cardiac death.
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PMID:Cardiac prognosis in hypertensive patients. Incidence of sudden death and ventricular arrhythmias. 334 89

Vasodilator substances act either directly on vascular smooth muscle (e.g., adenosine) or indirectly (e.g., acetylcholine) on endothelial cells that respond by releasing an unknown powerful, short-lived relaxing factor. To determine whether chronic hypertension or hypercholesterolemia or both would alter the release of the endothelium-derived relaxing factor, experiments were performed in hypertensive rabbits (5-week cellophane wrap perinephritis; mean blood pressure, 134.7 mm Hg) and normotensive rabbits (mean blood pressure, 80 mm Hg) with a Doppler flow transducer and perivascular balloon implanted on the lower abdominal aorta. Rabbits were fed either 1% cholesterol or control diet for 4 weeks before the experiment. On the day of the experiment, resting hindlimb vascular resistance was greatest in hypertensive rabbits fed 1% cholesterol diet, followed (in descending order) by hypertensive rabbits, normotensive rabbits fed 1% cholesterol diet, and normotensive rabbits. Pharmacological autonomic reflex blockade was induced, and steady state intravenous infusion curves to acetylcholine, serotonin, and adenosine were constructed. Sensitivity (location of effective dose, 50%) to the three vasodilator agents was altered less than twofold from the values in normotensive rabbits for any treatment group. The maximum vasodilator response to acetylcholine, but not to adenosine or serotonin, infusion was reduced significantly in the treated rabbits compared with that in normal rabbits. Reactive hyperemic responses to 5 to 80 seconds of ischemia were not significantly different among the treatment groups. These results indicate that hypertension with or without hypercholesterolemia does not greatly alter the responsiveness of the hindlimb resistance vasculature to these three vasodilator agents or to ischemia.
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PMID:Effects of hypertension and hypercholesterolemia on vasodilatation in the rabbit. 369 79


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