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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To establish the relation between treadmill exercise testing and ambulatory St segment monitoring in the detection of ischemia in patients with coronary artery disease, and to assess whether standard medical therapy affects any such relation, 277 patients with stable angina and angiographically documented coronary artery disease were studied with treadmill exercise testing and 48 h ambulatory ST segment monitoring. One hundred forty-six patients (52%) were studied while receiving no routine antianginal therapy, and 131 (48%) while receiving standard medical therapy. In 187 patients (67%) the exercise test was positive for ischemia. During 11,964 h of ambulatory monitoring, 881 episodes of ischemia (645 [73%] silent) were recorded, of which 809 (92%) occurred in patients with a positive exercise test. The mean heart rate at the onset of ischemic episodes during ambulatory monitoring was significantly less than that at the onset of 1 mm ST segment depression during exercise testing (94.5 versus 105.9 beats/min, p less than 0.0001). However, the frequency of ambulatory ischemic episodes was strongly related to a positive exercise test (p less than 0.001), and this relation was similar for both silent and painful ischemia (p less than 0.0001 for both) and in patients who were and were not receiving therapy (p less than 0.0001 for both). The total duration of ischemia was similarly related to a positive exercise test (p less than 0.0001). Only one patient with a negative exercise test had frequent (greater than 5/day) episodes of ischemia on ambulatory monitoring and had documented coronary artery spasm. Thus, exercise testing identifies the majority of patients likely to have significant ischemia during their daily activities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ischemia in the ambulatory setting--the total ischemic burden: relation to exercise testing and investigative and therapeutic implications. 280 69

The diagnosis of coronary artery spasm is confirmed by angiography, for example, change in caliber of the coronary arteries plus evidence of ischemia. The prevalence and contribution of coronary artery spasm in the individual patient with symptoms of ischemic heart disease is not known and depends on how the condition is defined. The prognosis of patients with coronary artery spasm appears to depend on the presence or absence of severe coronary atherosclerosis, that is, those with severe disease have a worse prognosis. Nitrates should be used to initiate therapy in all patients with this problem. Intravenous nitrates have proven useful in patients whose symptoms are difficult to control and who require hospitalization. beta blockers used alone may be detrimental in patients with coronary artery spasm, but studies supporting the detrimental effects are few. The combination of nitrates, beta blockers and nifedipine has proved effective therapy for many patients with recurrent angina at rest, possibly related to coronary artery spasm. Several open-label and double-blind placebo control trials have shown that all of the calcium antagonists are effective short-term agents for patients with proven coronary artery spasm. When nifedipine was compared with isosorbide dinitrate in a randomized crossover, double-blind trial in patients with coronary artery spasm, both drugs were shown to be efficacious and neither was superior. The traditional alpha-blocking agents have not been shown to be an effective therapy, but a recent study of prazosin, a selective alpha blocker, revealed excellent results in patients whose conditions were resistant to therapy with traditional calcium blockers, beta blockers and, in 1 case, phenoxybenzamine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Large vessel coronary vasospasm: diagnosis, natural history and treatment. 285 17

In conclusion, the PIA patient is at high risk, with higher early as well as late mortality. The pathophysiology of PIA is complex and may vary from patient to patient. The concepts of ischemia at a distance and ischemia in the infarct zone have led to a better understanding of early PIA. Coronary spasm may play an important role in most PIA patients as in the general population of patients with angina pectoris. Medical therapy is efficacious in many, although it may on rare occasion aggravate myocardial ischemia. Urgent coronary arteriography is generally safe and should be performed as soon as possible for medically refractory PIA. CABG appears to be safe in experienced hands, but its timing must be individualized. The IABP should be reserved for more unstable patients for fear of vascular complications. Randomized controlled trials such as the BARI Trial will further compare PTCA with CABG.
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PMID:Postinfarction angina. 288 57

Coronary artery spasm unresponsive to intracoronary nitroglycerin was observed in eight patients undergoing percutaneous transluminal coronary angioplasty for unstable ischemic symptoms (unstable angina or recent nontransmural infarction, or both). All patients manifested eccentric lesions angiographically with the right coronary artery involved in four, circumflex artery in two and left anterior descending in two. Severe coronary spasm was documented angiographically in all patients after angioplasty and resulted in symptomatic and electrocardiographic evidence of ischemia. Multiple sites of spasm were present in the dilated vessel in three patients. Coronary artery spasm persisted despite the infusion of large doses of intracoronary nitroglycerin (200 to 2,000 micrograms, mean 850 micrograms) over 10 min. Administration of intracoronary verapamil (1 to 1.5 mg over 10 min) resulted in complete relief of spasm with restoration of brisk anterograde flow in all patients. These findings suggest that intracoronary verapamil may be a useful agent for the relief of coronary spasm occurring in the setting of coronary angioplasty.
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PMID:Intracoronary verapamil for reversal of refractory coronary vasospasm during percutaneous transluminal coronary angioplasty. 297 6

Injury to the endothelial lining of arteries is an important mechanism in both the early and late stages of the development of atherosclerosis. Platelets can contribute to the early lesions by releasing factors that cause smooth muscle cell migration and proliferation. In the later stages, the formation of large platelet-fibrin thrombi that become organized into the vessel wall contributes to the development of focal atherosclerotic narrowing of arteries. Injury to the vessel wall can also be a factor in causing spasm of coronary arteries, particularly at sites of stenosis. The spasm may cause ischemia, anginal pain, and, in some individuals, ventricular fibrillation and death. In other individuals, the spasm may not cause death but may persist long enough for an occlusive thrombus to form and cause myocardial infarction. The events leading to thrombosis involve not only the release of arachidonic acid and the formation of TXA2, but other pathways that are independent of the arachidonate pathway. In some circumstances thrombin (which causes platelet aggregation and release that are largely independent of the arachidonate pathway and TXA2 formation) is the primary stimulus causing the initiation and growth of the thrombus. The role of products of the arachidonate pathway in causing spasm is not understood. PGI2 produced by the vessel wall could be important in preventing or minimizing coronary artery spasm. The best way to prevent the development of atherosclerosis and its clinical complications is to prevent or minimize injury of the endothelium.
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PMID:Platelets, endothelium, and vessel injury. 315 7

In the absence of fixed coronary artery disease, thyrotoxicosis is rarely associated with acute myocardial infarction and/or ischemia. There are no known reports on the association of acute myocardial infarction with iatrogenic or factitious thyrotoxicosis in the absence of fixed coronary artery stenosis or coronary artery spasm. A 68-year-old woman, clinically in a state of thyrotoxicosis as a result of taking 0.3 g/d of exogenous thyroid replacement, sustained a severe, reversible myocardial ischemic event. Echocardiographic and scintigraphic evaluations demonstrated a large apical dyskinetic region. Subsequently, after the original dose of levothyroxine sodium was reduced to 0.15 mg and the patient became euthyroid, two-dimensional echocardiography and scintigraphic and cardiac catheterization studies demonstrated normal left ventricular contractility and normal coronary anatomy. Coronary artery spasm was not induced by ergonovine maleate therapy. Exogenous thyroid administration may directly influence myocardial oxygen supply and demand, exclusive of coronary artery disease and coronary spasm. A critical imbalance may then result in acute myocardial ischemia and reversible left ventricular segmental wall motion abnormalities.
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PMID:Myocardial infarction, severe reversible ischemia, and shock following excess thyroid administration in a woman with normal coronary arteries. 337 27

Five patients, all women in their 50s and all with a documented history of migraine headaches, had ischemic chest pains investigated. Four patients had angina primarily occurring at rest, with documented ischemic electrocardiographic changes during pain in all five. Three subjects sustained myocardial infarction, one shortly after taking ergotamine tartrate for an acute attack of migraine. Subsequent coronary angiography in all five subjects revealed no evidence of atherosclerotic coronary artery disease, suggestive of spasm as the cause of ischemia. In subjects with known migraine, the occurrence of chest pain may represent coronary artery spasm, and should be investigated with concurrent electrocardiographs, as these two clinical entities may be related as part of a generalised vasospastic disorder. The use of ergot preparations should be contraindicated in such patients, as exacerbation of chest pain and frank myocardial infarction may result. These chest pains responded favourably to calcium channel blockers.
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PMID:A possible relationship between migraine and coronary artery spasm. 346 72

Myocardial perfusion scintigraphy with 201-TL was performed in a group of subjects affected by exercise-induced, rate-dependent left bundle branch block (LBBB). The aim of the study was: to define the significance of the exercise-induced conduction abnormality: "primitive" or "ischemic". 14 patients, aging 28-58 years (x = 42), 8 with chest pain (4 typical angina, 4 atypical angina) and 6 without any symptoms were studied. None had history of prior myocardial infarction or clinical and echocardiographic signs of heart disease. LBBB appeared at a heart rate ranging from 70 to 160 beats/min. 6 patients showed repolarization abnormalities (ST changes, deep and negative T wave) suggestive for ischemia, during successive QRS normalization. 201-TL-uptake was normal in 5 subjects; in the remaining 9 ones reversible TL defects were demonstrated in the septum (6), in the septum and apex (2), in the septum and inferior-apical wall (1). No patients had irreversible impaired perfusion. All the patients had normal coronary angiography, with negative ergonovine test for coronary artery spasm. In conclusion, in the majority of our subjects (64%) with exercise-induced LBBB, a reversible TL-uptake defect, usually located in the septum without diagnostic value of obstructive CAD, has been observed. Further studies will establish if the TL-defect is only an "apparent phenomenon" due to contraction abnormality secondary to LBBB, or, on the contrary, an expression of myocardial ischemia with normal coronary vessels as a consequence of the LBBB.
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PMID:[Study of myocardial perfusion by means of scintigraphy with thallium-210 in left bundle branch block induced by exertion]. 366 78

Myocardial ischemia, particularly when transmural as in variant angina pectoris, may be associated with ventricular tachycardia, ventricular fibrillation and paroxysmal atrioventricular block (15%). Syncope (7%) and sudden death (3%) due to these malignant arrhythmias are sometimes a unique marker of myocardial ischemia. Two-hundred fifty-four patients (220 males and 34 females), aged 5 +/- 9 years with transmural myocardial ischemia related to coronary artery spasm, were studied. Particular attention was paid to the role of syncopal attacks as unique clinical manifestation of silent ischemia. Patients examined were divided into 3 Groups. Group 1 includes 5/254 (2%) patients with atrial fibrillation during acute ischemia. Group 2 was divided into four subgroups: subgroup A includes 17/254 (7%) patients with syncopal attacks due to malignant arrhythmias (ventricular tachycardia and advanced A-V block); subgroup B, 15/254 (6%) patients with documented malignant arrhythmias, without syncopal attacks; subgroup C, 7/254 (3%) with ventricular fibrillation during acute ischemia and subgroup D, 18/254 (7%) patients with history of syncopal attacks without documented arrhythmias during hospital observation. Group 3 includes 17/254 (7%) patients with left anterior hemiblock in basal condition, 7/254 (3%) patients with left anterior hemiblock and one left posterior hemiblock during acute ischemia and one patient with right bundle branch block during acute ischemia. Syncopal symptoms are present in many of these cases of angina pectoris; paroxysmal A-V block is documented in nearly half of the cases with syncope (65%); ventricular tachycardia is frequently demonstrated during ischemia but leads to syncope in only a few cases; patients with syncope do not present specific clinical features.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:When are arrhythmias and conduction disturbances markers of myocardial ischemia at rest? 375

Left ventricular ejection fractions and regional ejection changes obtained from left ventriculograms at rest were analyzed in 15 normal subjects, in 17 patients with isolated, organic left anterior descending coronary artery disease, and in 11 patients with isolated left anterior descending coronary artery spasm. Patients with coronary artery spasm did not have significant organic lesions at the site of spasm. All patients with organic coronary artery disease and coronary artery spasm had a history of angina pectoris without myocardial infarction. No significant differences in ejection fraction were observed among the three groups. The regional ejection change of the anterolateral and apical wall supplied by the left anterior descending coronary artery was significantly decreased in patients with organic coronary artery disease compared with those in normal subjects (anterolateral 39.5 +/- 10.3% vs 48.4 +/- 7.7%, p less than 0.05; apical 48.4 +/- 8.8% vs 55.6 +/- 7.8%, p less than 0.05). However, the anterolateral and apical wall motion was not impaired in patients with coronary artery spasm. Thus, patients with organic coronary artery disease had impairment of left ventricular wall motion, while those with coronary artery spasm did not, although both groups of patients had symptoms of angina. These results suggest that patients with organic coronary artery disease may have had coronary blood flow disturbances through stenosed vessels and chronic active ischemia that produced left ventricular impairment.
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PMID:Left ventricular wall motion at rest in patients with organic coronary artery disease vs coronary spasm. 382 58


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