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 order to determine the natural evolution of different clinical types of "unstable angina", 167 patients were included in a prospective study. After angiography, 11 (6.5%) were excluded because they had no significant coronary lesions. The remaining 156 were sorted into different groups according to their clinical characteristics and were followed up for a period of 24 months at least. After that follow-up period, mortality and incidence of acute myocardial infarction (AMI) were as follows: angina of recent onset (Class III--IV NYHA): 8.5% (3/35) and 34.2% (12/35). Progressive angina: 7.4% (2/27) and 7.4% (2/27). Intermediate syndrome: 41.6% (10/24) and 37.5% (9/24). Prinzmetal's angina: 10% (1/10) and 10% (1/10). Post acute myocardial infarction angina: 35% (7/20) and 10% (2/20). Acute persistent ischemia: 2.5% (1/40) and 20% (8/40). Comparison of these figures pointed out significant differences (p less than 0.001 for mortality and p less than 0.03 for AMI incidence respectively). We conclude that it is clinically possible to identify different groups within the so-called unstable angina. Such a division not only allows for the creation of more homogeneous groups, but it contributes to a more rational therapeutic approach and also permits identification of high risk prodromes of greater complications, such as myocardial infarction or sudden death.
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PMID:Clinical spectrum of "unstable angina". 26 65

71 patients undergo myocardial revascularisation for Prinzmetal's angina; among them, 50 p. cent are operated upon in emergency according to three ways of anaesthesia: neuroleptanalgesia, analgesic anaesthesia, combined anaesthesia. The authors lay stress on the importance of per- and post-operative complications: electrocardiographic ischemia in 22 p. cent of the cases, severe ventricular excitability perturbations were observed in 21 p. cent, myocardial necrosis in 14 p. cent, cardiovascular collapse in 21 p. cent and hypertensions in 22 p cent. These complications are often associated. In the discussion, the authors underline anesthetic induction as a cause of Prinzmetal's angina in 50 p. cent of the cases. They put the accent on the severity of peroperative crisis followed in 50 p. cent of the cases by serious ventricular excitability perturbations. In 25 p. cent of the cases myocardial necrosis is a complication of the spasm of a coronary artery. In this field, posterior necrosis are more frequent and correspond to the spasm of the right coronary artery. All the patients of this series, except one, develop necrosis in the spastic area (by-passed or not). Per-operative hypertension has no incidence on the occurrence of post-operative complications. Lastly, continuous per-operative infusions of nitroglycerine has been performed in several patients in order to reduce morbidity of this type of surgery.
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PMID:[Prinzmetal's angina during myocardial revascularisation. Cardiovascular complications in 71 patients (author's transl)]. 31 82

Prinzmetal's variant angina is commonly referred to as a syndrome apart from the usual spectrum of atherosclerotic disease. 2 well-studied patients with this form of angina gave past histories compatible with classical angina. They were found to have, in addition to severe atheromatous lesions, coronary artery spasm resulting in complete obstruction of the vessel during Prinzmetal attacks. The concomitant electrocardiographic ST segment elevations are probably the reflection of transmural ischemia injury resulting from the transient complete occlusion of the corresponding coronary artery. Electrocardiograms taken during milder resting anginal attacks showed minimal nonspecific changes of the electrocardiogram or T wave inversions which may possibly reflect less severe ischemia, secondary to milder coronary spasm. These observations support the possibility that at least in some cases, Prinzmetal's angina may just be a phase in the life history of patients with atherosclerotic disease, during which recurrent severe coronary spasms may occur.
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PMID:Another look at Prinzmetal's variant angina. 91 86

We compared patients with variant angina (ST-segment elevation during pain) who had normal or near normal coronary arteriograms (Group 1) with 20 in whom variant angina occurred in the presence of obstructive coronary lesions (Group 2). A long history of nonexertional angina without angina of effort or previous infarction was the rule in Group 1, whereas recent-onset unstable angina preceded by effort angina and infarction predominated in Group 2 (P less than 0.001). Normal electrocardiograms at rest, with ischemic ST-segment elevation in the inferior leads, and ischemia-induced heart block and bradycardia, characterized Group 1, whereas abnormal electrocardiograms, ischemic involvement or fibrillation were more common in Group 2 (P less than 0.001). Variant angina with normal coronary arteriogram generally has a benign course and is probably unrelated to atherosclerosis.
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PMID:Clinical syndrome of variant angina with normal coronary arteriogram. 98 80

A relationship of coronary arterial spasm to variant angina pectoris, subendocardial ischemia, major ventricular arrhythmias and myocardial infarction has been demonstrated. In 29 patients, spasm was angiographically observed in normal-appearing coronary arteries (7 patients) as well as superimposed on various degrees of coronary atherosclerotic obstruction (22 patients). All patients experienced an atypical anginal syndrome;16 patients also experienced typical exertional angina. Coronary spasm appeared to be a major contributory factor in eight occurrences of myocardial infarction and in 11 incidents of ventricular tachycardia, ventricular fibrillation and heart block. Coronary spasm in the 29 cases was distributed in the following fashion: left main trunk, 6 cases; right main trunk, 12 cases; proximal left anterior descending artery, 13 cases; proximal circumflex artery, 1 case; distal left anterior descending artery, 1 case; and distal circumflex artery, 2 cases. In 5 cases coronary spasm was noted at multiple sites.
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PMID:Spectrum of coronary arterial spasm. Clinical, angiographic and myocardial metabolic experience in 29 cases. 99 29

The purpose of this study is to determine why precordial ST elevation (V1 lead) occurs during acute occlusion of the right coronary artery (RCA). Nineteen patients with vasospastic angina, in whom ergonovine administration into RCA provoked spasms, were divided into 2 groups by precordial ST change during spasms. Group I (n = 6) had precordial ST elevation; group II (n = 13) had no precordial ST elevation. A subgroup, IIA was comprised 6 patients in group II with spasms in the RCA proximal segment (segment number less than 2 of AHA coronary classification). None had left coronary dominancy. There was no difference in collateral flow during spasms. Location of spasms in group I was in the RCA proximal segment, and was significantly more proximal compared to group II. There was no difference in sigma ST in II, III, aVF between group I and II or IIA. Max ST elevation time by which duration of ischemia was estimated was significantly longer in group I than in group IIA. Three patients in group I displayed precordial ST depression before elevation, in all of whom in sigma ST in II, III, aVF was higher during precordial ST elevation than during depression. During acute occlusion in the RCA proximal segment, precordial ST elevation is caused by ischemia of the right ventricular anterior wall. Furthermore, precordial ST elevation can occur in a patient with RCA dominance, even if ischemic injury in the left ventricular infero-posterior wall increases progressively.
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PMID:Precordial ST segment elevation in acute ischemia caused by right coronary artery occlusion. 140 44

Traditionally, myocardial ischemia has been viewed as an imbalance in the supply and demand of myocardial oxygen. Stable angina is usually considered to involve a fixed lesion, whereas unstable angina involves a fixed lesion as well as such components as platelet aggregation, thrombotic processes, and vasospasm. Variant angina involves primarily vasospasm. A newer concept holds that most angina results from mixed mechanisms in which both fixed lesions and vasomotor alterations play a role. These mechanisms are responsible for mixed ischemic events, characterized by episodes at varying levels of exertion, with or without anginal pain. This concept would seem to be supported by the occurrence of silent ischemia in the setting of stable, unstable, or variant angina, despite differing pathophysiologic conditions. Ischemic events have important prognostic significance; unfortunately, many are unrecognized by patients. The question whether the treatment of ischemic events will improve prognosis remains a matter of debate.
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PMID:Mechanisms of myocardial ischemia. 144 93

The relationship between silent myocardial ischemia and sudden death depends on the severity and duration of the ischemia. Severe, transmural and persistent ischemia, as occurs in myocardial infarction, can trigger sudden death. When the ischemia is severe and transmural but not long-standing (e.g., Prinzmetal angina), ventricular arrhythmias appear frequently, but they are rarely malignant. In cases of subendocardial ischemia, there is no definitive proof of this relationship.
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PMID:Do silent myocardial ischemia and ventricular arrhythmias interact to result in sudden death? 150 75

A 60-year-old man with atypical chest pain not submitted to adequate diagnostic procedures was treated on an empirical basis with nifedipine 20 mg b.i.d. The patient was referred to our institution where a first symptom-limited exercise stress-test during treatment was performed; neither S-T alterations nor clinical symptoms were induced at the maximal tolerated work load. Therefore we suggested a short period of hospital stay to repeat the stress-test after a progressive tapering off of the drug with the aim of obtaining a more definite diagnosis. However the patient refused and an at-home nifedipine withdrawal was planned. Some days later a second test showed marked S-T segment elevation in leads V4 to V6; concomitant high-grade ventricular arrhythmias and anginal pain occurred. Both the ECG alterations and the clinical symptom promptly regressed interrupting the test and administering sublingual isosorbide dinitrate. A coronary angiography performed few days later showed only a single and no significant stenosis of the left anterior descending artery (60%). The clinical and electrocardiographic pictures were therefore attributed to stress-induced vasospastic ischemia. A week later a third maximal stress-test during further treatment with nifedipine was totally negative. The pathophysiological mechanisms of rest and stress-induced vasospastic angina and the usefulness of Ca-blocking agents are discussed.
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PMID:[A clinical case: coronary vasospasm induced by exercise after stopping nifedipine therapy]. 163 Jun 75

We examined whether recurrent transient ischemia may effect left ventricular systolic and diastolic function or not. Left ventricular systolic and diastolic function during the asymptomatic period was studied by gated radionuclide ventriculography (RNV) in 25 patients with vasospastic angina (VA) who had no significant coronary stenosis, in 25 patients with effort angina (EA), and in 20 controls (C). There was no significant difference among patients in all three groups in regards to systolic indices (Ejection Fraction, Peak Ejection Rate). But diastolic indices (Peak Filling Rate, Time to Peak Filling Rate, 1/3 Mean Filling Rate, 1/3 Filling Fraction) were impaired not only in patients with EA but also in patients with VA. The treatment with nitrates and/or Ca antagonist for 6-24 months did not bring about any changes in these data concerning systolic and diastolic function in patients with VA. Thus, it is suggested that the diastolic function is impaired in patients with VA even during the asymptomatic period, though systolic function remains normal. Recurrent transient ischemia may cause irreversible myocardial injury.
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PMID:[Impairment of left ventricular diastolic function during the asymptomatic period in vasospastic angina patients without significant coronary stenosis]. 174 68


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