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)

In patients with severe coronary disease and poor left ventricular function, coronary artery bypass grafting has a positive impact on long-term survival. In presence of angina or documented ischemia, it is beneficial in protecting functioning muscle against future infarction. In patients with heart failure and no angina, it is a rational option when large areas of akinetic but viable myocardium are identified preoperatively; under these circumstances, recovery of myocardial function is the goal of coronary revascularization. Obviously, reliable methods of assessing myocardial viability and contractile reserve are required for an accurate selection of patients. Advances in perioperative management, including myocardial preservation, have consistently reduced the operative risk in the most recent series, and more appropriate selection criteria have substantially contributed to the improved long-term survival. Variables associated with higher hospital mortality as well as factors influencing long-term outcome have been identified. The beneficial effect of coronary artery bypass grafting on the functional status of patients has been documented in several studies, and the improvement in left ventricular function has been objectively demonstrated. The concepts and the data presented in this review may help to define the present role of coronary artery bypass grafting in the treatment of ischemic cardiomyopathy.
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PMID:Coronary artery bypass grafting for left ventricular dysfunction. 781 24

Previous studies have pointed out that congestive heart failure (CHF) with normal ejection fraction presents a uniform clinical profile that is indistinguishable from heart failure with low ejection fraction. Thirty-six patients with systemic hypertension who had recently experienced CHF with normal ejection fraction (> or = 50%) and no clinical history of ischemic cardiomyopathy were studied. The patients were divided into 2 groups according to degree of echocardiographic hypertrophy: group A (19 patients) with a ventricular mass/volume ratio > 1.8, and group B (17 patients) with a ratio < 1.8. Group A patients had a higher ejection fraction (67 +/- 6 vs 57 +/- 3%, p < 0.01), smaller ventricular diameters and a lower thallium-201 positive rate at peak stress (10 vs 70% in group B, p < 0.001), with 8 of 10 showing severe coronary stenosis. Clinically, group A had a more frequent audible fourth sound (79 vs 17%, p < 0.001), a low incidence of audible third sound (5 vs 55%, p < 0.001) and a cardiothoracic ratio < or = 0.5 (63 vs 17%, p < 0.01). The degree of radionuclide-detected resting diastolic dysfunction and exercise intolerance was similar in both groups. In conclusion, CHF with normal ejection fraction in hypertensive patients presents 2 different profiles: one characterized by severe hypertrophy and the other by a high rate of myocardial regional ischemia. Therapy should be aimed at pathophysiologic regression of the hypertrophy in the first case, and at improvement of the ischemia in the second.
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PMID:Congestive heart failure from left ventricular diastolic dysfunction in systemic hypertension. 842 73

Identifying preserved myocardial viability in the presence of severe regional left ventricular dysfunction is becoming increasingly more important for clinical decision-making to better select those patients with coronary artery disease who will benefit most from revascularization. 201Tl remains the most commonly employed radionuclide for detecting both ischemia and viability. A post-exercise defect showing complete or partial redistribution on delayed images implies transient ischemia and preserved viability with a 90% chance of exhibiting improved 201Tl uptake with repeat testing after coronary revascularization. Mild persistent defects with < 50% 201Tl uptake on 4-hour redistribution images also imply viability with a 60-70% probability of showing improved 201Tl uptake after repeat imaging following revascularization with concomitant enhancement of regional systolic function. In contrast, a severe persistent defect with < 50% 201Tl uptake compared to peak uptake has only a 15% chance of exhibiting improved perfusion and corresponding improved function after revascularization. Detection of defect reversibility on 201Tl imaging is enhanced by "reinjection" of a second 201Tl dose after acquisition of redistribution images. Initial and 4-hour rest/redistribution imaging has proven most useful for detection of viability in the resting state in patients with ischemic cardiomyopathy. The greater the extent of preoperative viability, the greater is the improvement in regional and global function after revascularization. 99mTc sestamibi has also been demonstrated to be extracted by myocardial cells in proportion to regional blood flow in the presence of viable myocites. Although this agent does not redistribute after intravenous injection, its > 50% uptake of the tracer implies viability and predicts improved regional function after revascularization. Finally, positron emission tomography with 18F fluorodeoxyglucose (FDG) is perhaps the most sensitive noninvasive imaging technique for detection of viability in stunned or hibernating myocardium. A mismatch pattern between regional flow and FDG uptake has approximately an 80-85% positive predicted value for predicting improved function in asynergic myocardial regions after revascularization. A match pattern where flow and FDG uptake are both reduced has an 80% negative predicted value for lack of functional recovery after revascularization.
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PMID:Assessment of myocardial perfusion and metabolism for assessment of myocardial viability. 868 Oct 14

Several potential manifestations and outcomes are associated with myocardial ischemia and reperfusion. When ischemia is severe and prolonged, irreversible damage occurs and there is no recovery of contractile function. When ischemia is less severe or shorter in duration, recovery of contraction may occur instantaneously or more commonly, after considerable delay, which is the condition recognized as "stunned myocardium." Stunning is defined as a transient left ventricular dysfunction that persists after reperfusion despite the absence of irreversible damage and restoration of normal or near-normal coronary flow. Oxidative stress and alteration of calcium homeostasis during reperfusion are the probable causes of stunning. Clinically, stunning may occur after acute infarction, successful thrombolysis, unstable angina, angioplasty, resolution of coronary spasm, open-heart surgery, or transplantation. It can be treated with interventions aimed at prevention or reversal. When ischemia is prolonged but less severe, myocytes may remain viable but exhibit depressed contraction. Under these conditions, reperfusion restores normal contractile performance. This type of ischemia, leading to a reversible, chronic left ventricular dysfunction, has been termed "hibernating myocardium." The intrinsic mechanisms of this condition are unknown. Clinically, it is very important to diagnose hibernation because reperfusion of the hibernating myocardium by angioplasty or heart surgery restores contraction, and this correlates with long-term survival. A number of methods are available to access the hibernating myocardium. These include cardiac imaging techniques that evaluate myocardial viability, such as positron emission tomography and thallium myocardial imaging, or methods that evaluate contractile reserve, such as low-dose dobutamine echocardiography. Interestingly, reperfusion of patients with end-stage ischemic cardiomyopathy and hibernating myocardium can be considered an alternative to transplantation.
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PMID:Left ventricular dysfunction due to the new ischemic outcomes: stunning and hibernation. 889 67

Experiments in animal models of myocardial infarction have provided evidence that early magnesium infusion can limit the infarct size. One mechanism that has been postulated to be of importance is a protection of the cardiomyocyte against a calcium overload during or after ischemia. We had shown that in isolated human myocytes from patient with ischemic cardiomyopathy an increase of the extracellular magnesium concentration could block the L-type-calcium current in a dose dependent manner. Until recently only small, uncontrolled studies have indicated there may be a reduction of mortality due to myocardial infarction when intravenous magnesium infusion was added to standard therapy. However, two recently published randomized studies showed different results, although similar doses of magnesium were used (70-80 mmol magnesium over 24 h). The LIMIT-2-study was a double-blind, placebo controlled investigation of over 2300 patients with suspected myocardial infarction. Magnesium infusion was associated with a reduction of the 28 day mortality by 24%. The ISIS-4-study on over 50,000 patients with suspected myocardial infarction did not show any positive effect of magnesium on mortality. Major differences between both studies were differences in thrombolysis (LIMIT-2:1/3, ISIS-4: 70%). Furthermore, in LIMIT-2 magnesium infusion was started as early as possible, whereas in ISIS-4 magnesium was given after the end of thrombolytic therapy. In can be concluded that magnesium therapy in acute myocardial infarction after thrombolytic therapy is not useful. However, in patients where thrombolytic therapy is not feasable, early infusion of magnesium may be beneficial. As side effects are minor and costs are low, a therapeutic trial may be warranted, although a final decision on the effects of magnesium cannot be made.
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PMID:[Value of magnesium in acute myocardial infarct]. 906 57

To determine the cardiovascular protective effects of angiotensin-converting enzyme inhibitors, we examined the response to intensive vasodilator therapy in patients with ischemic cardiomyopathy and ongoing angina pectoris. We found that for patients with ischemic cardiomyopathy and ongoing active angina, intensive vasodilator therapy with angiotensin-converting enzyme inhibition and nitrates improved not only heart failure-related symptoms, but also resulted in a significant improvement in symptomatic ischemia and ischemia-related morbid events.
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PMID:Response of symptomatic myocardial ischemia in ischemic cardiomyopathy to intensive vasodilator therapy. 923 Jan 64

Both dobutamine stress echocardiography (DSE) and myocardial perfusion scintigraphy are used to assess myocardial viability. Few studies have compared the data on myocardial viability and ischemia by low and peak dose DSE and myocardial perfusion imaging in the same patients. Fifty-four patients (45 men and 9 women aged 65 +/- 9 years) with ischemic cardiomyopathy (mean ejection fraction 24 +/- 9%) underwent rest 4-hour redistribution thallium-201 single-photon emission computed tomography (SPECT), low and peak dose DSE, and dobutamine sestamibi SPECT. A total of 864 segments were analyzed (16 segments/patient). Wall motion abnormality was present in 796 segments (92%), and contractile reserve during dobutamine infusion was seen in 400 of these segments (50%). Contractile reserve was seen in 331 of 509 hypokinetic segments (65%) and 69 of 287 akinetic/dyskinetic segments (24%) (p <0.001). Contractile reserve was more frequent in segments with normal thallium uptake (64%), reversible thallium defects (42%), or mild to moderate fixed thallium defects (48%) than severely fixed defects (22%) (p <0.05 each). Concordant information about viability by thallium imaging and DSE was obtained in 62% of segments. Dobutamine sestamibi ischemia was seen in 518 of 796 segments (65%) compared with 265 segments (33%) by DSE (p <0.001). Scintigraphic ischemia was noted in 126 of 195 segments (65%) demonstrating biphasic response, 129 of 205 segments (63%) showing sustained improvement, 42 of 70 segments (60%) deteriorating during dobutamine infusion, and 221 of 326 (68%) demonstrating no change (p = NS). Thus, in patients with ischemic cardiomyopathy, contractile reserve is more frequent in hypokinetic segments than akinetic/dyskinetic segments. The number of segments with normal or near-normal thallium uptake or with scintigraphic ischemia is significantly greater than the number of those capable of increasing contractile function or demonstrating an ischemic response during dobutamine echocardiography.
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PMID:Comparison of dobutamine echocardiography, dobutamine sestamibi, and rest-redistribution thallium-201 single-photon emission computed tomography for determining contractile reserve and myocardial ischemia in ischemic cardiomyopathy. 1049 29

We sought to identify mechanisms for chronic dysfunction in hibernating myocardium. Pigs were instrumented with a left anterior descending artery stenosis for 3 mo. Angiography demonstrated high-grade stenoses and hibernating myocardium with 1) severe anterior hypokinesis (P < 0.001 vs. shams), 2) reduced subendocardial perfusion [0.73 +/- 0.05 (SE) vs. 1.01 +/- 0.06 ml. min(-1). g(-1) in normal, P < 0.001], and 3) critically reduced adenosine flow (1.0 +/- 0.17 vs. 3.84 +/- 0.26 ml. min(-1). g(-1) in normal, P < 0.001). Histology did not reveal necrosis. Northern blot analysis of hibernating myocardium demonstrated regional downregulation in mRNAs for sarcoplasmic reticulum (SR) proteins phospholamban (0.76 +/- 0.08 vs. 1.07 +/- 0.06, P < 0.02) and SR Ca(2+)-ATPase (0.83 +/- 0.06 vs. 1.02 +/- 0.06, P < 0.05) with no change in calsequestrin (1.08 +/- 0.06 vs. 0.96 +/- 0.05, P = not significant). Heat shock protein (HSP)-70 mRNA was regionally induced in hibernating myocardium (2.4 +/- 0.3 vs. 1.0 +/- 0.11, P < 0.01). Directionally similar changes were confirmed by Western blot analysis of respective proteins. Our results indicate that hibernating myocardium exhibits a molecular phenotype that on a regional basis is similar to end-stage ischemic cardiomyopathy. This supports the hypothesis that SR dysfunction from reversible ischemia may be an early defect in the progression of left ventricular dysfunction.
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PMID:Regional alterations in SR Ca(2+)-ATPase, phospholamban, and HSP-70 expression in chronic hibernating myocardium. 1051 77

Blood vessels are essential for the supply of oxygen and nutrients to the heart. An imbalance between oxygen demand and supply (ischemia), as occurs when coronary arteries become obstructed by atherosclerotic plaques, triggers a response to improve myocardial perfusion by the formation of new capillaries (angiogenesis) and by the enlargement of preexisting collateral vessels (arteriogenesis). Recently, novel insights have been obtained in the molecular mechanisms of angiogenesis and in its control by hypoxia. This has lead to the design of strategies to improve myocardial perfusion. However, rational design of therapeutic angiogenesis mandates a better understanding of the molecular basis of angiogenesis. This review discusses the role of two prime classes of angiogenic molecules, namely of vascular endothelial growth factor (VEGF) and angiopoietin (Ang), and addresses novel insights in the regulation of angiogenesis by hypoxia. In addition, a novel mouse model of ischemic cardiomyopathy with signs of hibernation is presented. Possible implications for therapeutic myocardial angiogenesis are discussed.
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PMID:Basic Concepts of (Myocardial) Angiogenesis: Role of Vascular Endothelial Growth Factor and Angiopoietin. 1109 39

This article summarizes the clinical and biochemical evidence for maximal treatment of atherosclerosis by a simultaneous 60% to 70% reduction of plasma low-density lipoprotein cholesterol (LDL cholesterol), fibrinogen, and lipoprotein a concentrations with heparin-mediated extracorporeal LDL/fibrinogen precipitation (HELP) apheresis and statins. Apheresis has proven efficient and safe in the treatment of more than 1,000 patients since 1984 and has been applied in children and adults for the treatment of homozygous and heterozygous familial hypercholesterolemia, coronary artery disease, ischemic cardiomyopathy, generalized atherosclerosis, or transplant-associated arteriosclerosis after cardiac transplantation. Simultaneous removal of the main atherogenic plasma compounds has an immediate impact on myocardial and peripheral vasomotion by increasing myocardial blood flow, coronary flow reserve, cerebral CO2-reactivity, and muscle oxygen tension. Removal of fibrinogen and cholesterol reduces plasma viscosity by 20% and erythrocyte aggregation by 60% which gives rise to applying the HELP apheresis in various microcirculatory disorders. Pilot studies on acute retinal ischemia, critical limb ischemia, and sudden hearing loss confirm this observation.
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PMID:Evidence for maximal treatment of atherosclerosis: drastic reduction of cholesterol and fibrinogen restores vascular homeostasis. 1146 57


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