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 variable prognosis after myocardial infarction necessitates an individual tailoring of follow-up treatment. Therapeutic decisions must be based on a complete risk stratification including assessment of persisting ischemia, left ventricular function, rhythmic instability and cardiovascular risk factor profile. High risk patients (prognostic indication) as well as symptomatic patients (symptomatic indication) should be referred for coronary angiography to assess the need for revascularisation procedures (PTCA, CABG). The individual risk profile also defines drug therapy for secondary prevention (not more than 3-4 drugs): anti-platelet agents or anticoagulation in every patient; beta blockers in all but the lowest risk group; ACE-inhibitors in heart failure or asymptomatic, substantial left ventricular dysfunction; liberal use of cholesterol-reducing drugs. Life style alterations should be encouraged in almost every patient. Information about the necessary measures to be taken upon occurrence of angina at rest or other cardiac symptoms must be repeatedly given to all patients.
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PMID:[After care of acute myocardial infarct: what are the 4 most important points?]. 932 21

The purpose of this study was to evaluate risk factors predicting restenosis and primary patency after percutaneous transluminal angioplasty. Follow-up data (including cardiovascular risk factor scores according to SCVIR criteria, preinterventional and postinterventional clinical data and patient history) of all patients who underwent successful percutaneous transluminal angioplasty for lower limb ischemia were analyzed retrospectively and patients, relatives, or referring physicians underwent a telephone interview. Patients with incomplete follow-up data were examined by means of a clinical examination, including Doppler measurements and treadmill test. Additionally all angiograms were evaluated to calculate lesion length, number of treated lesions, lesion type (SCVIR score), and runoff. The outcome was categorized into four groups: early recurrence (< 1 month, group I), mean recurrence (1-6 months, group II), late recurrence (>6 months, group III), and no recurrence (group IV). According to common concepts group I was defined as early (thrombotic) reocclusion, group II as clinically defined restenosis, and group III as progression of atherosclerosis. One hundred thirty-seven patients underwent percutaneous transluminal angioplasty of 148 extremities. The groups differ significantly only with respect to a higher diabetes score for group I in comparison to group IV (p=0.002, Kruskal-Wallis test), and a worse runoff of group I compared with group IV (p =0.008). There was a trend toward a higher diabetes score for group II in comparison to group IV (p = 0.014). There were no differences with regard to hyperlipemia, hypertension, and tobacco use between patient groups. Mean primary patency was 436 days. Predictors for lower patency rates were diabetes mellitus (p<0.001), runoff (p=0.005), and number of treated lesions (p=0.007) in a stepwise, multiple regression analysis. Patients with clinically defined restenosis showed no specific risk factor profile in this study. Predictors for lower primary patency were diabetes mellitus, number of treated lesions, and runoff.
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PMID:Cardiovascular risk factors do not predict clinically defined restenosis after percutaneous transluminal angioplasty for lower limb ischemia. 1186 5

Type II secretory phospholipase A2 (sPLA2) is a cardiovascular risk factor. We recently found depositions of sPLA2 in the necrotic center of infarcted human myocardium and normally appearing cardiomyocytes adjacent to the border zone. The consequences of binding of sPLA2 to ischemic cardiomyocytes are not known. To explore a potential effect of sPLA2 on ischemic cardiomyocytes at a cellular level we used an in vitro model. The cardiomyocyte cell line H9c2 or adult cardiomyocytes were isolated from rabbits that were incubated with sPLA2 in the presence of metabolic inhibitors to mimic ischemia-reperfusion conditions. Cell viability was established with the use of annexin V and propidium iodide or 7-aminoactinomycin D. Metabolic inhibition induced an increase of the number of flip-flopped cells, including a population that did not stain with propidium iodide and that was caspase-3 negative. sPLA2 bound to the flip-flopped cells, including those negative for caspase-3. sPLA2 binding induced cell death in these latter cells. In addition, sPLA2 potentiated the binding of C-reactive protein (CRP) to these cells. We conclude that by binding to flip-flopped cardiomyocytes, including those that are caspase-3 negative and presumably reversibly injured, sPLA2 may induce cell death and tag these cells with CRP.
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PMID:Type II secretory phospholipase A2 binds to ischemic flip-flopped cardiomyocytes and subsequently induces cell death. 1280 18

Findings of diminished or absent pulses, pallor on elevation, redness of the foot on lowering of the leg, sluggish refilling of the toe capillaries, and thickened nails or absence of toe hair are consistent with impaired arterial perfusion to the foot. When ischemia is recognized as contributing to pedal ulceration and infection in the diabetic foot, quantitation of its severity may be difficult. Standard clinical evaluation of trophic changes is limited in an infected foot with its accompanying swelling, edema, and erythema. A palpable pedal pulse does not preclude the possibility of the presence of limb-threatening ischemia. Additional non-invasive vascular studies should be undertaken for these patients. Management of the diabetic foot is often a complex clinical problem. However, the principles of care are simple, including correction of systemic factors, such as blood glucose control, cardiovascular risk factor management, and smoking, as well as local factor correction, such as debridement, pressure relief, infection control, and revascularization when indicated. When a patient presents with evidence of infection, adequate drainage and antibiotic therapy are mandatory. The next step should be performed to differentiate the more common neuropathic ulcerations from the truly ischemic ulceration. Symptoms of rest pain or claudication are not often helpful because many of these patients are asymptomatic as a result of the presence of their neuropathy and inactivity. If an infected foot requires debridement or open partial forefoot amputation, observing the wound on a daily base is also important. Once infection is eradicated, there should be prompt signs of healing, including the development of wound granulation within several days. If wounds are not showing signs of prompt healing, arteriography is necessary. Early aggressive drainage, debridement, and local foot amputations combined with liberal use of revascularization results in cumulative limb salvage of 74% at 5 years in high-risk groups. Others report that pedal bypass to the ischemic infected foot is effective and safe as long as infection adequately controlled. These studies strongly suggest that early recognition and aggressive surgical drainage of pedal sepsis followed by surgical revascularization is critical to achieving maximal limb salvage in the high-risk population. Patients who have diabetes present a unique challenge in lower extremity revascularization because of the distal origination of many bypasses, distal distribution of the occlusive disease, and the frequently calcified arterial wall. An aggressive multidisciplinary approach to foot disease associated with diabetes involving the primary care provider, medical specialists, interventional radiology, and podiatric, plastic, and vascular surgeons will provide optimal medical and surgical care. Peripheral vascular disease is highly treatable if intervention is instituted in a timely and collegial fashion.
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PMID:Vascular evaluation and arterial reconstruction of the diabetic foot. 1463 33

Although hypercholesterolemia is widely accepted as a major risk factor for coronary artery and peripheral vascular diseases, its role in the pathogenesis of stroke is controversial. The objectives of this study were to determine how hypercholesterolemia affects the cerebral microcirculation under resting conditions and after ischemia-reperfusion (I/R). Platelet- and leukocyte-endothelial cell interactions and oxidant production (using the oxidant-sensitive fluorochrome dihydrorhodamine-123) were monitored by intravital videomicroscopy in the cerebral microvasculature of mice placed on either a normal (ND) or cholesterol-enriched diet (HCD). Platelets labeled with carboxyfluorescein diacetate succinimidyl ester (CFDASE) and leukocytes labeled with rhodamine 6G were seen to roll and firmly adhere, with a corresponding increase in oxidant production, in venules of mice on HCD, but not ND. Immunoneutralization of P-selectin attenuated the platelet- and leukocyte-endothelial cell interactions and the enhanced oxidant production associated with HCD. A GPIIb/IIIa blocking antibody did not alter the blood cell-vessel wall interactions to HCD. Mice deficient in the NADPH oxidase subunit gp91(phox) exhibited significantly blunted platelet and leukocyte recruitment responses to HCD. Focal I/R also elicited inflammatory and prothrombogenic responses in cerebral venules and these were exaggerated in mice on HCD. These results implicate an oxidant-dependent, P-selectin-mediated mechanism in the blood cell-vessel wall interactions induced by hypercholesterolemia in the brain and demonstrate that the deleterious effects of I/R on the brain are exacerbated by this cardiovascular risk factor.
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PMID:Cerebral microvascular responses to hypercholesterolemia: roles of NADPH oxidase and P-selectin. 1467 Aug 46

Insulin-like growth factor-1 (IGF-I), the primary mediator of growth hormone (GH) effects, is an important regulator of cell growth, differentiation, and apoptosis. GH and IGF-I deficiency is known to be associated with premature atherosclerosis and elevated cardiovascular disease mortality. Recent evidence suggests that cardiovascular disease risk may also be elevated among apparently healthy individuals who have serum IGF-I levels in the low-normal range. In this review, we appraise the epidemiologic and clinical studies implicating low IGF-I level as a risk factor for incident myocardial infarction and other manifestations of coronary heart disease. Potential mechanisms that may underlie this association include beneficial effects of IGF-I on myocyte survival after ischemia, stability of atherosclerotic lesions, and endothelial function. We conclude that additional confirmatory data from prospective studies are needed to confirm low IGF-I level as an independent cardiovascular risk factor. However, if this finding is confirmed, this would support the rationale for intervention trials aimed at reducing cardiovascular disease morbidity and mortality among older adults by targeting the GH/IGF-I pathway.
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PMID:Insulin-like growth factors and coronary heart disease. 1559 27

A 51-year-old woman had no known cardiovascular risk factor. She presented with bilateral calf intermittent claudication from February. She was hospitalized in August for acute right leg ischemia without loss of sensorymotor functions, following angiography by one week. She had an occlusion of both superficial femoral arteries and abdominal aorta thrombus, plausible source for embolism. Her condition quickly improved with heparin and iloprost infusion. Since the aortic thrombus was removed on ultrasound, aortic surgery was not performed at this time. Investigations showed hyperhomocysteinemia (25 microg/L after overnight fasting and 115 after methionin load) and decrease in folic acid. This report highlights the occurrence of severe arterial disease in young women with high serum homocysteine levels.
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PMID:[Subacute ischemia of the lower limb revealing hyperhomocysteinemia in a young woman]. 1614 82

Accelerated atherosclerosis in dialysis patients is characterized by severe vascular calcification, and the magnitude of vascular calcification is associated with increased cardiovascular mortality. Calcification-dependent arterial stiffness is considered to be a major determinant of cardiac failure in uremia. Fetuin-A/alpha(2)-Heremans-Schmid glycoprotein is an abundant serum protein with powerful calcification inhibitory properties. Fetuin-A deficiency was recently linked to cardiovascular mortality in dialysis patients. Fetuin-A knockout (fetuin-KO) mice spontaneously develop widespread soft tissue calcification, including significant myocardial calcification, whereas larger arteries are spared. Therefore, this investigation offers the unique opportunity to study the functional role of isolated myocardial calcification independent of arterial stiffness by assessing the hemodynamics of fetuin-KO mice. Cardiac output in fetuin-KO mice was lower than in wild-type mice (fetuin-KO 1.81 +/- 0.18 versus WT 2.45 +/- 0.29 ml/min per g; P < 0.005), and fetuin-KO mice were refractory to dobutamine stimulation. Left ventricular relaxation was significantly impaired in fetuin-KO hearts with the relaxation index reduced by 23% (P < 0.005). After ischemia, fetuin-KO hearts displayed a continuous decline in left ventricular developed pressure after the initial phase of reperfusion, resulting in 77 +/- 15% of preischemic left ventricular developed pressure (P < 0.05 versus wild-type). In fetuin-KO mice, dystrophic cardiac calcification, with myocardial calcium contents increased 60-fold, was associated with profound induction of profibrotic TGF-beta and downstream collagen and fibronectin mRNA synthesis. In conclusion, independent of arterial stiffness, calcification-associated "myocardial stiffness" characterized by cardiac fibrosis, diastolic dysfunction, impaired tolerance to ischemia, and catecholamine resistance thus may constitute an underestimated cardiovascular risk factor that contributes to cardiac failure in calcification-prone states.
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PMID:Myocardial stiffness, cardiac remodeling, and diastolic dysfunction in calcification-prone fetuin-A-deficient mice. 1617

Morbidity and mortality of peripheral arterial occlusive disease significantly increases with age, often exhibiting more severe disease pathology and decreased treatment effectiveness. Therapeutic angiogenesis with angiogenic growth factors may represent a valuable treatment option for the severely ill, older adult patient population. Aging is considered an independent cardiovascular risk factor, but pathomechanistically it is not well understood. Diminished endothelial nitric oxide (EDNO) production has been considered as a major contributor to the aging process. To investigate the effect of age on postischemic revascularization independent of changes in EDNO, we used endothelial nitric oxide synthase-deficient (ecNOS-KO) mice. We found an age-dependent acceleration in ischemic injury following unilateral femoral artery ligation in these animals compared to C57BL/J6 mice. Postischemic revascularization, quantified by measuring von Willebrand factor expression, was significantly impaired, suggesting that factors other than progressive EDNO deterioration are also involved in the age-dependent severe disease phenotype. Ischemia led to an increase in the expression of vascular endothelial growth factor receptor-2, KDR, in younger ecNOS-KO; however, this increase in KDR expression was absent in the older animals. Lack of increased KDR expression may provide a mechanistic explanation for the severe ischemic injury and perhaps can be used as a clinical marker to identify severe, vascular endothelial growth factor refractory patient population.
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PMID:Age-dependent acceleration of ischemic injury in endothelial nitric oxide synthase-deficient mice: potential role of impaired VEGF receptor 2 expression. 1668 73

A 35-year-old woman was hospitalized for subacute ischemia of the left leg following an intermittent claudication for some weeks. She also presented paleness and coldness of both hands. The radial pulses could not be palpated. Smoking was the only cardiovascular risk factor. Duplex ultrasonography and angiography revealed a left popliteal thrombus combined with low diameter leg arteries and in the upper limbs stenosis of the left radial artery and thrombosis of the right radial artery. Search for a metabolic, embolic or thrombophilic etiology was negative. More minute history taking revealed use of cannabis and recent nasal administration of cocaine. Her condition improved with heparin therapy except for the upper limbs with ischemia of the hands and disabling Raynaud's phenomenon. This report highlights the combined arterial toxicity of drugs often used together by drug addicts. The association of cannabis use and tobacco smoking is not rare in patients with Buerger-like juvenile arteriopathy and cocaine may provoke peripheral vascular disease by embolism or in situ thrombosis. Interrogation of a patient presenting with Buerger-like peripheral arterial disease should insist on detecting use of drugs in association with tobacco smoking.
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PMID:[Sub acute ischemia of a lower limb in a patient with juvenile peripheral arterial disease and arterial cocaine toxicity]. 1673 38


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