Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the validity of Gradient recalled EPI(GRE-EPI) after bolus injection of contrast agent(Gadolinium 0.1 mmol/kg) to detect the ischemic zone of myocardium. Seven healthy volunteers and fifteen patients with coronary artery disease who had only one vessel disease more than 99% stenosis in AHA/ACC classification were studied. GRE-EPI was performed in a transaxial, long axis or short axis orientation of the left ventricle on a 1.5-T Signa Horizon Scanner. Images were obtained every heartbeat for 200 consecutive heartbeats. Contrast agent was injected into the antecubital vein in a bolus after 10 heartbeats. Signal intensity changes in the left ventricular blood and myocardium were measured during myocardial contrast perfusion study. In all healthy volunteers, signal intensity in myocardium was reduced by contrast agent following signal loss in the left ventricular blood and recovered with wash out of contrast agent. But in patients, reduction and recovery of signal intensity in the ischemic zone by contrast agent were significantly delayed and much less than that in the nonischemic zone. In conclusion, myocardial perfusion imaging with GRE-EPI was useful in evaluation of ischemic heart disease.
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PMID:[Evaluation of myocardial ischemia with echo planar magnetic resonance imaging (EPI): normal and ischemic heart]. 923 34

Sildenafil citrate is the first orally active therapy proved to be effective and safe treatment for erectile dysfunction (ED). Because men with cardiovascular disease are at increased risk of developing ED, and because ED and cardiovascular disease share important risk factors, attention has focused recently on the use of sildenafil in these men. When used in combination with nitroglycerin and other nitric oxide (NO) donors, sildenafil may potentiate major drops in blood pressure. Use of nitrate antianginal agents are an absolute contraindication to sildenafil use. In normotensive men and in men receiving antihypertensive medications evaluated in Phase II/III clinical trials, sildenafil use at the recommended doses (25-100 mg 1 hour before sexual intercourse and no more than once daily) was associated with modest, transient reductions in blood pressure and negligible effects on heart rate. In a more recent study, sildenafil was well tolerated in patients receiving antihypertensive medications and was not associated with major decreases in blood pressure. From the time of its approval in the United States in March 1998 through mid-November 1998, with approximately 6 million prescriptions written, 130 deaths were reported by the US Food and Drug Administration (FDA). Seventy-seven of the men who died had documented cardiovascular events. Sixteen men took or were administered nitroglycerin or an organic nitrate; 3 others had nitroglycerin in their possession. Physician prescribing guidelines issued by the American College of Cardiology/American Heart Association (ACC/AHA) recommend caution when prescribing sildenafil to men with certain cardiovascular conditions, liver or kidney disease, and to those taking medications that may prolong sildenafil's half-life (e.g., erythromycin or cimetidine). Those with known or suspected coronary artery disease may benefit from an exercise test to determine whether resumption of sexual activity with use of sildenafil is likely to be associated with an increased risk of myocardial ischemia.
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PMID:Cardiovascular effects of sildenafil citrate and recommendations for its use. 1050 71

The recent document of the ESC/ACC Committee for the redefinition of myocardial infarction (MI) has introduced the measurement of cardiac troponin as the biochemical standard for the diagnosis of MI. This change has been mainly driven by the demonstration that any amount of myocardial damage, as detected by cardiac troponins, implies a worse long-term outcome of the patient. The results of several studies consistently show that there is a continuous relationship between the degree of troponin elevation and the patient's prognosis. The new definition has important consequences on the diagnostic and therapeutic approaches to patients with acute coronary syndromes; in fact, patients with increased troponins, i.e. patients with MI, necessitate more aggressive treatment than those without troponin elevations, i.e. patients with unstable angina. The application of the new definition is expected to increase the number of cases of MI by about 30% and to decrease mortality. We believe that several aspects of the new definition need to be discussed before the new criteria for MI are used in clinical practice in Italy. The most relevant issues are the following: 1) the definition of troponin elevation should meet the analytical performance of the available assays, the diagnostic cutoff of which is frequently too imprecise. We propose that troponin elevations be defined as values exceeding the concentration corresponding to a total analytical imprecision of 10%. We disclose such a concentration for the currently available assays and suggest its use in clinical practice to mitigate the possibility of false-positive values; 2) the number of samples required for the diagnosis should be sufficient for the assessment of the changes in concentration over time. When only one sample is available, or when the temporal pattern of the changes in marker concentration is not consistent with the time elapsed from the onset of symptoms, we suggest that objective evidence that myocardial ischemia is the likely cause of myocardial damage should be obtained; 3) the diagnosis of MI after a percutaneous coronary intervention represents a unique situation. In contrast with myocardial damage occurring during spontaneous ischemia, available data do not support the concept that any troponin elevation is associated with an adverse prognosis. In the absence of conclusive studies, we suggest that the diagnosis of MI after a percutaneous coronary intervention be based on conventional criteria. Finally, we propose this summary with the aim of overcoming some of the more controversial aspects of the ESC/ACC redefinition of MI: Criteria for acute, evolving or recent MI. Either one of the following criteria satisfies the diagnosis for an acute, evolving or recent MI: 1) elevation of biochemical markers of myocardial necrosis (preferably troponin) with at least one of the following: a) ischemic symptoms; b) development of pathologic Q waves on the ECG; c) ECG changes indicative of ischemia (ST segment elevation or depression); d) coronary artery intervention (e.g., coronary angioplasty). Marker elevations should be accompanied by objective evidence that myocardial ischemia is the likely cause of myocardial damage when: a) only one blood sample is available; b) marker changes over time are not consistent with the onset of symptoms; 2) pathologic findings of an acute MI. Criteria for established MI. Anyone of the following criteria satisfies the diagnosis for established MI: 1) development of new pathologic Q waves on serial ECGs. The patient may or may not remember previous symptoms. Biochemical markers of myocardial necrosis may have normalized, depending on the length of time that has passed since the infarct developed; 2) pathologic findings of a healed or healing MI.
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PMID:The new definition of myocardial infarction: analysis of the ESC/ACC Consensus Document and reflections on its applicability to the Italian Health System. 1240 56

The recent document of the ESC/ACC Committee for the redefinition of myocardial infarction (MI) has introduced the measurement of cardiac troponin as the biochemical standard for the diagnosis of MI. This change has been mainly driven by the demonstration that any amount of myocardial damage, as detected by cardiac troponins, implies a worse long-term outcome of the patient. The results of several studies consistently show that there is a continuous relationship between the degree of troponin elevation and the patient's prognosis. The new definition has important consequences on the diagnostic and therapeutic approaches to patients with acute coronary syndromes; in fact, patients with increased troponins, i.e. patients with MI, necessitate more aggressive treatment than those without troponin elevations, i.e. patients with unstable angina. The application of the new definition is expected to increase the number of cases of MI by about 30% and to decrease mortality. We believe that several aspects of the new definition need to be discussed before the new criteria for MI are used in clinical practice in Italy. The most relevant issues are the following: 1) the definition of troponin elevation should meet the analytical performance of the available assays, the diagnostic cut-off of which is frequently too imprecise. We propose that troponin elevations be defined as values exceeding the concentration corresponding to a total analytical imprecision of 10%. We disclose such a concentration for the currently available assays and suggest its use in clinical practice to mitigate the possibility of false-positive values; 2) the number of samples required for the diagnosis should be sufficient for the assessment of the changes in concentration over time. When only one sample is available, or when the temporal pattern of the changes in marker concentration is not consistent with the time elapsed from the onset of symptoms, we suggest that objective evidence that myocardial ischemia is the likely cause of myocardial damage should be obtained; 3) the diagnosis of MI after a percutaneous coronary intervention represents a unique situation. In contrast with myocardial damage occurring during spontaneous ischemia, available data do not support the concept that any troponin elevation is associated with an adverse prognosis. In the absence of conclusive studies, we suggest that the diagnosis of MI after a percutaneous coronary intervention be based on conventional criteria. Finally, we propose this summary with the aim of overcoming some of the more controversial aspects of the ESC/ACC redefinition of MI: Criteria for acute, evolving or recent MI. Either one of the following criteria satisfies the diagnosis for an acute, evolving or recent MI: 1) elevation of biochemical markers of myocardial necrosis (preferably troponin) with at least one of the following: a) ischemic symptoms; b) development of pathologic Q waves on the ECG; c) ECG changes indicative of ischemia (ST segment elevation or depression); d) coronary artery intervention (e.g., coronary angioplasty). Marker elevations should be accompanied by objective evidence that myocardial ischemia is the likely cause of myocardial damage when: a) only one blood sample is available; b) marker changes over time are not consistent with the onset of symptoms; 2) pathologic findings of an acute MI. Criteria for established MI. Anyone of the following criteria satisfies the diagnosis for established MI: 1) development of new pathologic Q waves on serial ECGs. The patient may or may not remember previous symptoms. Biochemical markers of myocardial necrosis may have normalized, depending on the length of time that has passed since the infarct developed; 2) pathologic findings of a healed or healing MI.
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PMID:[New definition of myocardial infarction: analysis of the consensus document ESC/ACC and thoughts about applicability to the Italian health situation]. 1240 66

AMP-activated protein kinase (AMPK) is emerging as a key signaling pathway that modulates cellular metabolic processes. In skeletal muscle, AMPK is activated during exercise. Increased myocardial substrate metabolism during exercise could be explained by AMPK activation. Although AMPK is known to be activated during myocardial ischemia, it remains uncertain whether AMPK is activated in response to the physiological increases in cardiac work associated with exercise. Therefore, we evaluated cardiac AMPK activity in rats at rest and after 10 min of treadmill running at moderate (15% grade, 16 m/min) or high (15% grade, 32 m/min) intensity. Total AMPK activity in the heart increased in proportion to exercise intensity (P < 0.05). AMPK activity associated with the alpha2-catalytic subunit increased 2.8 +/- 0.4-fold (P < 0.02 vs. rest) and 4.5 +/- 0.6-fold (P < 0.001 vs. rest) with moderate- and high-intensity exercise, respectively. AMPK activity associated with the alpha1-subunit increased to a lesser extent. Phosphorylation of the Thr172-regulatory site on AMPK alpha-catalytic subunits increased during exercise (P < 0.001). There was no increase in Akt phosphorylation during exercise. The changes in AMPK activity during exercise were associated with physiological AMPK effects (GLUT4 translocation to the sarcolemma and ACC phosphorylation). Thus cardiac AMPK activity increases progressively with exercise intensity, supporting the hypothesis that AMPK has a physiological role in the heart.
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PMID:Physiological role of AMP-activated protein kinase in the heart: graded activation during exercise. 1275 23

Four hundred and ten patients with ischemic heart disease (IHD) were treated. The study group consisted of 197 patients with IHD who have undergone intracoronary stenting (IS). The control group consisted of 213 patients treated with traditional balloon coronary angioplasty (BCA). All the patients in both groups were divided in four subgroups depending on a type of stenosis by classification ACC/AHA. A positive angiographic and clinical result straight away after IS was seen in all 197 patients. Any links with a stenosis type or with construction of the stent were not revealed. In 5 (2.5%) patients on day 5-7 after IS acute coronary occlusion in the place of stenting was seen. In 2 (1%) patients attempt of recanalization was unsuccessful, in both cases transmural myocardial infarction has developed. Thus, in further study 195 (98.98%) patients were included. Out of 213 patients after traditional BCA immediate good angiographic and clinical results were achieved in 191 (89.7%). There were no differences in rate of good immediate results of IS and BCA of types A and B1 stenoses. In types B2 and C stenosis immediate good results were achieved more often in group with IS. Good immediate results after BCA were better in patients with type A stenosis than with B2 and C stenoses. Rate of the "stent-like" result after BCA of types A and B1 stenosis was higher than after dilatation of types B2 and C stenosis. There was no difference in rate of restenosis after traditional BCA and IS of types A and B1 stenosis. In BCA of types B2 and C stenosis restenosis was seen more often than in IS. It is concluded that in patients with types A and B1 stenoses "stent-like" result is achieved more often after traditional BCA than in patients with types B2 and C stenosis. In patients with type A stenosis and "stent-like" result stenting does not improve significantly long-term results. In patients with types B2 and C stenosis and "stent-like" result IS is tustified. Good immediate results of angioplasty in these patients don't reduce the rate of restenosis, white IS does reduce its rate.
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PMID:[Indications to balloon angioplasty and intracoronary stenting in patients with ischemic heart disease]. 1286 19

Perioperative cardiac event is relatively high in vascular surgery for arteriosclerosis obliterans (ASO), which is a major cause of postoperative death. ACC/AHA guideline and revised cardiac risk index (CRI) were advocated to assess risk factor stratification and to manage risk reduction. ACC/AHA guideline categorized all vascular procedures except carotid endarterectomy as high risk. Because almost all patients with ASO were aged and/or inactive, noninvasive testing was necessary in almost all patients by the stepwise bayesian strategy. Patients with revised CRI less than 1 point dominated about three fourths of all patients, whose prevalence and incidence of ischemic heart disease (IHD) were 2.5% and 1.3%, respectively. It seemed appropriate to apply noninvasive testing only for patients with revised CRI more than 2 points, and high risk indicated coronary angiography. Electrocardigrams obtained at baseline, immediately, and on the first 2 days after surgery appear to be cost-effective to diagnose IHD. Use of cardiac biomarkers was reserved for patients at high risk and those with clinical, or ECG evidence of myocardial infarction (MI). Beta-blockers or alpha-agonists were effective to reduce incidence of perioperative IHD. Although even optimal preoperative assessment and perioperative management, some patients will have perioperative MI.
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PMID:[Perioperaive evaluation and management in vascular surgery especially for arteriosclerosis obliterans]. 1593 52

Ischemic heart disease is one of the leading causes of death in Japan. Acute coronary syndrome (ACS) most commonly begins with atherosclerotic plaque rupture and intracoronary thrombus formation. Therefore, the primary goal of treatment of acute coronary occlusion is the achievement of early and complete reperfusion. To achieve this goal, detection of atherosclerosis and/or myocardial necrosis by imaging and serologic tests is important. Original diagnosis of acute myocardial infarction (AMI) was made from typical symptoms, characteristic rises in serum enzyme levels, and an atypical electrocardiographic pattern. Increasingly sensitive and specific tests have been developed in recent years and have been rapidly adopted into clinical practice. Rapid developments in technology in the field of serum biomarkers have redefined the diagnosis of AMI. The new ESC/ACC criteria place increased emphasis on cardiac biomarkers, especially troponins. However, the electrocardiogram still remains significant in the diagnosis of AMI and the ability to identify high risk subgroups by admission electrocardiogram is necessary to estimate the severity of AMI. Current practice guidelines recognize the importance of promptly restoring normal epicardial blood flow, but blood flow to the ischemic tissue may still be impeded after relief of the occlusion; a phenomenon known as no reflow. Myocardial scintigraphy is one of the methods for defining coronary microvascular injury in the acute phase of AMI. Prompt assessment of coronary perfusion and detection of coronary microvascular injury may aid in making decisions concerning the use of drugs to improve microvascular function and left ventricular function after primary coronary angioplasty.
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PMID:[Ischemic heart disease]. 1596 7

One of the first signs of ischemic heart disease may manifest as chronic stable angina, a mismatch between oxygen supply and demand. With more than approximately 16.5 million people each year having stable angina, development of new therapies to help control this disease state are warranted. Ranolazine, a novel agent exerting its effect through a partial fatty oxidase inhibitor, is one of the first new drugs in more than 20 years to be developed for chronic stable angina. Working through enzymatic modulation, instead of altering myocardial hemodynamics, ranolazine appears to be effective. An overview of chronic stable angina is provided, the American College of Cardiology-American Heart Association (ACC-AHA) current pharmacologic treatment guidelines are reviewed, and the mechanism of action of ranolazine is explored. Finally, the major clinical trials supporting its place in medical therapy are discussed. Additional clinical trials are under way to further elucidate ranolazine's exact role in the treatment of chronic stable angina. From results of the existing phase III clinical trials, however, the most beneficial potential role of ranolazine in the treatment algorithm of chronic stable angina appears to be as adjunctive therapy to the recommended ACC-AHA treatment modalities.
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PMID:Ranolazine, a novel agent for chronic stable angina. 1650 55

Pharmacological therapy for acute coronary syndrome (ACS) is divided into the treatment for myocardial ischemia and that for coronary thrombosis. Immediate nitrates(sublingual tablets and sprays) are used to alleviate attacks and patients not responding them are treated by intravenously in 24 hours. The initial treatment for non-ST-segment elevation myocardial infarction(NSTEMI) with the administration of nitrates and beta blocker is judged as Class I (evidence level B) by ACC/AHA classification. Administering beta blocker in patients with ACS has reduced the progression to myocardial infarction by 13%. Ca antagonist is administered in patients for whom nitrates and/or beta blocker are contraindicated or in whom myocardial ischemia persists or frequently relapses in spite of the treatment with an adequate dose of the drugs. Since recent studies have suggested that ACS may not result from a local vascular stenosis, but from coronary inflammation, treating the local vascular lesion alone with PCI is not enough. Rather, pharmacological therapy is important to reduce overall patient risk, thereby suppressing the progress of atherosclerosis.
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PMID:[Anti-anginal medication in management of acute coronary syndrome]. 1661 94


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