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)

To determine if maximal exercise treadmill testing influences the occurence of ventricular arrhythmia in the hours after exercise, 45 myocardial infarction and 22 angina pectoris patients (New York Heart Association Class I-II), and 23 normal subjects were examined with 24-hour ambulatory electrocardiographic Holter recordings before and after exercise testing. Comparison of qualitative and quantitative ventricular arrhythmia detected during identical chronological two-, four-, and 20- or more hour periods, before and after exercise testing in each patient, revealed no statistically significant difference in any patient group. The prevalence of ventricular ectopy in 80 per cent of ischemic heart disease patients and 30 per cent of normal subjects as detected by 24-hour Holter recordings was similar to previous studies. It is concluded that in ambulatory ischemic heart disease patients (New York Heart Association Class I-II) and normal subjects, maximal treadmill testing does not significantly affect the occurrence of ventricular arrhythmia in the hours after exercise.
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PMID:Ventricular arrhythmia 24 hours before and after maximal treadmill testing. 33 63

The clinical significance of the abnormalities seen at left ventriculography in ischaemic heart disease is discussed. Aneurysms may be recognized when left ventriculography is combined with coronary arteriography to show the characteristic obliteration of the supplying artery. Localized areas of abnormal contraction seen at rest are almost certainly indicative of infarcts. Similar areas provoked by exercise or atrial pacing represent the site of acute ischaemia. The ischaemic ventricle may be recognized by abnormal response to exercise, even in the absence of angina. The abnormal response may be reversed by successful revascularization surgery.
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PMID:Left ventricular function in ischaemic heart disease. A review. 34 80

Suspecting that platelet thromboemboli could play a role in the pathogenesis of myocardial ischemia, we did a random-order, double-blind, crossover study of the effect of the platelet aggregation inhibitor, aspirin, on treadmill exercise-induced angina in 13 men with coronary artery disease. Although collagen-induced platelet aggregation and the second phase of adenosine diphosphate (ADP)-induced platelet aggregation were significantly decreased and the rate of disaggregation of ADP-induced platelet aggregates was significantly increased after 650 mg aspirin in buffered solution, there was no delay in onset of exercise-induced angina, change in heart rate-blood pressure product at onset of angina, or change in S-T segment depression at onset of angina. Regardless of whether the patients had received placebo or aspirin on the preceding day, treadmill exercise until angina was followed by no changes in platelet aggregation or disaggregation, platelet count in blood or platelet-rich plasma, or of the plasma concentration of nonesterified fatty acids.
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PMID:Effect of aspirin on exercise-induced angina. 34 92

The relation between global and regional left ventricular function and electrocardiographic signs of ischemia at rest and during submaximal supine exercise was studied in 27 patients 2 to 3 weeks after acute myocardial infarction. Dynamic myocardial scintigraphy was performed at rest and during submaximal exercise utilizing an in vivo method of labeling red blood cells with technetium-99m pertechnetate. Gated radionuclide blood pool scintigrams were obtained in a modified left anterior oblique, and in some patients also in the right anterior oblique projection, to measure left ventricular ejection fraction and segmental wall motion. Electrocardiographic monitoring of heart rate and rhythm was provided during the exercise. The submaximal exercise test was terminated when the patient's heart rate reached 125 beats/min or if angina, malignant ventricular ectopy or electrocardiographic evidence of myocardial ischemia developed before this rate was reached. The data demonstrate that patients with a recent anterior myocardial infarct, in contrast to patients with a recent inferior or nontransmural infarct, manifest a significant reduction in left ventricular ejection fraction with submaximal exercise. Of the eight patients with an anterior infarct, seven had segmental wall motion abnormalities at rest. Four of these eight manifested more severe abnormalities with submaximal exercise; three had abnormalities at rest that did not change with exercise. Four of the eight had a positive electrocardiographic response during exercise (two were taking digoxin). Of these four, only two had more marked wall motion abnormalities with effort. Of the 13 patients with an inferior infarct, 11 had apparently normal wall motion in the modified left anterior oblique projection at rest, including 2 who manifested segmental wall motion abnormalities with submaximal exercise; the 2 remaining patients had wall motion abnormalities at rest that, on exercise, became more marked in one and were unchanged in one. Four of the 13 had a positive electrocardiographic response with exercise (one was taking digoxin); only one of these had a detectably more severe wall motion abnormality with exercise. Of the six patients with a nontransmural infarct, four had no identifiable wall motion abnormalities at rest; in one of these, an abnormality developed with exercise. The remaining two patients had wall motion abnormalities at rest; in one, a positive electrocardiographic ischemic response developed with exercise. Patients with an anterior infarct appear to have a different functional ventricular response to submaximal exercise at the time of hospital discharge than patients with an inferior or nontransmural infarct. To identify ischemic responses with submaximal exercise in these patients one should ideally use both electrocardiographic monitoring and dynamic myocardial scintigraphy.
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PMID:Submaximal exercise testing after acute myocardial infarction: myocardial scintigraphic and electrocardiographic observations. 35 68

William Heberden (1710--1801), in 1768, described angina pectoris, the classic symptom of ischemic heart disease, 150 years after the discovery of the coronary circulation by William Harvey (1578-1657). Another 110 years had elapsed before the first antemortem diagnosis (confirmed at autopsy) of coronary thrombosis was reported by Adam Hammer in 1878. The patient was a 34 year old man who died some 19 hours after a sudden collapse. Although the patient's clinical features were atypical (such as the absence of angina and the presence of complete heart block) and the autopsy showed vegetative aortic endocarditis that appeared to be causally related to the thrombotic coronary occlusion, Hammer's astute and carefully reasoned bedside diagnosis was history-making and deserves to be so recognized.
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PMID:Centenary of the first correct antemortem diagnosis of coronary thrombosis by Adam Hammer (1818--1878): English translation of the original report. 36 Aug 11

Coronary artery spasm is an important pathogenetic mechanism in some forms of myocardial ischemic disease. Factors that may be important in the genesis of spasm include the autonomic nervous system, prostaglandins, endoperoxides, thromboxanes, and the calcium availability to the contractile apparatus. Spasm results in myocardial ischemia with attendant chest pain and electrocardiographic and hemodynamic changes; it is the primary pathogenetic mechanism in Prinzmetal's variant angina and has been found in association with classic angina pectoris and acute myocardial infarction. Diagnosis of coronary artery spasm is firmly made only by coronary angiography. Treatment includes the use of both short- and long-acting nitrates and the slow-channel blocking agents such as verapamil, nifedipine, and perhexiline.
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PMID:Coronary artery spasm. 38 40

Coronary arterial vasoconstriction, well recognized in Prinzmetal's variant angina, may participate in the pathogenesis of classic angina as well. Several recent studies in patients with obstructive coronary artery disease suggest that apparently spontaneous reductions in coronary blood flow can result in myocardial ischemia and even infarction. Evidence supporting the alpha adrenergic nervous system as a cause of such coronary vasoconstriction is reviewed, particularly the results of provocative testing with the cold pressor stimulus. Upon exposure of the skin to cold, patients with coronary artery disease demonstrate an inappropriate coronary vasoconstrictor response, often sufficient to produce angina. Normal patients, by contrast, show no change in coronary vascular resistance. In patients with a diseases coronary circulation, inappropriate vasoconstriction further restricts myocardial perfusion and appears to be little affected by beta adrenergic blocking agents or nitrates in the usual dosages. Nifedipine has proved effective in preventing coronary arterial spasm in patients with Prinzmetal's angina. Studies currently in progress suggest that it is also effective in blocking inappropriate coronary vasoconstriction in patients with typical angina. Nifedipine may thus be a useful addition to the treatment of ischemic heart disease.
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PMID:Inappropriate coronary vasoconstriction in patients with coronary artery disease: a role for nifedipine? 38 63

Results with a new anti-angina molecule (nifedipine: Adalat) in the long-term management of 28 patients with ischaemic heart disease are presented. The effectiveness of the drug was judged outstanding on the strength of its reduction of angina outstanding on the strength of its reduction of angina crises and consumption of NTG beads. Non side-effects were noted.
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PMID:[Long-term clinical study of a new molecule (nifedipine) in ischemic cardiopathy]. 40 86

The applicability of the adenosine triphosphate (ATP) catabolites, inosine and hypoxanthine as markers of myocardial ischemia in humans with coronary artery disease has been investigated. Inosine and hypoxanthine were assayed enzymatically after separation by a new column chromatographic method. The myocardial lactate extraction at rest (17 +/- 13%) changed to production values (-23 +/- 28%) during pacing-induced angina (P less than 0.0005). Coronary venous inosine values increased from 535 +/- 185 nmol/l at rest to 1030 +/- 740 nmol/l during angina (P less than 0.005), the arterial values amounted to 770 +/- 325 nmol/l and 805 +/- 515 nmol/l respectively (P, NS). The calculated myocardial uptake of inosine at rest (27 +/- 16%) changed to production values (-25 +/- 29%) during angina (P less than 0.0005). Coronary venous hypoxanthine increased from 1000 +/- 760 nmol/l at rest to 1235 +/- 800 nmol/l during angina (P, NS), the arterial values amounted to 1300 +/- 1040 nmol/l and 1235 +/- 800 nmol/l respectively (P, NS). The myocardial extraction changed from 20 +/- 18% at rest to -5.4 +/- 29% during angina (P less than 0.0025). The significant positive correlation (r = 0.61, P less than 0.0025) between myocardial release and uptake of inosine and lactate during severe angina demonstrates that anaerobic glycolysis is accompanied by ATP breakdown. During a second pacing period at less increased pressure--rate product after nitroglycerin, lactate production (-1.7 +/- 22%) already occurred whereas extraction of inosine (19 +/- 19%) and hypoxanthine (24 +/- 15%) did not change. In conclusion, lactate functions as a sensitive marker of myocardial ischemia and inosine is useful in detecting ischemic myocardial energy deficiency by the indication of insufficient glycolytic ATP supply.
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PMID:Myocardial release of inosine, hypoxanthine and lactate during pacing-induced angina in humans with coronary artery disease. 42 23

The kinetics and dimensions of the septum and left posterior ventricular wall as well as left ventricular performance were investigated by echocardiography in 50 patients with painful ischemic heart disease. In 10 cases hypokinesia and low left ventricular performance were found, more marked in those with a history of angina pectoris and myocardial infarction. The utility of this technique for exploring myocardial contractility and its limits is discussed.
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PMID:Echocardiography in ischemic heart disease. 43 5


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