Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.1.6 (CAD)
 4,420 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 10 patients without and 20 patients with various degrees of angiographically proven CAD 93 pacing runs were studied. Changes of PAm, of ECG, and of anginal pain serving as parameters of myocardial ischemia were correlated to the rate-pressure-product. In patients without CAD no correlations could be ascertained. In each patient with CAD determination of ischemia was achieved reproducibly. Ischemia threshold is represented by a sharp increase of PAm. Ischemia threshold seems a parameter to be preferred as compared to pain threshold. The extent of CAD (angiographically estimated) correlates well with the pacing test especially when collaterals are taken into account. After NG no substantial improvement of ischemia can be detected: Ischemia threshold before and after NG was reached at same rate pressure in each case. We conclude the atrial pacing test to be an excellent test for the provocation of myocardial ischemia. The test is also useful for estimation of the extent of CAD.
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PMID:Pacing-induced myocardial ischemia in spite of nitroglycerin. Correlations regarding the extent of coronary artery disease. 80 82

Myocardial metabolism had been studied in 54 patients with continuous sampling of arterial (A) and coronary sinus (CS) blood during 8- to 10-min periods of control in sinus rhythm, rapid atrial pacing and recovery. The results showed that 17 subjects were normal or had insignificant coronary artery disease (CAD; nonischemic group = NI); 37 patients had significant CAD (ischemic group = 1) and developed clinical, hemodynamic, and electrocardographic evidence of myocardial ischemia during pacing, characterized by angina, elevated left ventricular end-diastolic pressure, and depressed ST segments. During pacing-induced ischemia the following metabolic abnormalities were detected: (1) myocardial anaerobiosis indicated by lactate % uptake ((A-CS)/AS X 100) of -17.2 +/- 5.0% (mean +/- SE); (2) myocardial loss of K+ suggested by an A-CS difference of -0.25 +/- 0.08 mEq/liter (N=18); (3) small but significant loss of inorganic phosphorus (Pi) of -1.0 +/- 1.4% (N=18); and (4) elevation of CS blood creatine phosphokinase activity (N=5). These metabolic abnormalities were temporally related to the other manifestations of myocardial ischemia and were not seen in the NI; Lactate production and Pi loss occurred in 75 and 55% of the IG, respectively, suggesting that accelerated anaerobic glycolysis was the best indicator of myocardial ischemia in man. K+ loss was an unreliable index in this experimental situation, since tachycardia alone caused significant K+ egress from the heart. Lactate production and K+ loss were reduced by nitroglycerin, which abolished angina and improved hemodynamics and electrocardiographic manifestations. That these metabolic abnormalities were not observed in all 1 patients may have been related to methodology, the random distribution of CAD, and the fact that the chemical composition of the CS blood reflects the metabolic balance of both well oxygenated and ischemic areas of the myocardium.
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PMID:Metabolic indicators of myocardial ischemia in man. 120 71

The clinical implications of isolated late recovery ST depression were tested in patients with scintigraphically defined ischemia (coronary artery disease [CAD], n = 18) compared with patients without ischemia (n = 25). Spontaneous (78.4 versus 12.0%, P < 0.008) and exercise-induced angina (44.4 versus 0%, P < 0.0001) were more frequently seen in patients with CAD. Histories of unstable angina (33.3%), prior myocardial infarction (27.8%), ST elevated angina (22.2%) and significant stenosis in the left anterior descending artery (17 of 18, 94.4%) were almost exclusively seen in the CAD group. There was no significant difference between the two groups in capacity for exercise, maximum deviation of ST level or TV2 amplitude. Balloon angioplasty abolished late recovery ST changes in 63.6% of CAD patients. These results suggest that isolated late recovery ST depression, when accompanied with typical chest pain, may be considered as an indicator of myocardial ischemia, but this phenomenon is difficult to distinguish electrocardiographically.
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PMID:Isolated post exercise delayed ST depression as a sign of severe ischemia: the influence of percutaneous transluminal coronary angioplasty. 128 36

Recent investigations of SMI occurring during daily life have advanced our understanding of the pathophysiology of myocardial ischemia. These contributions have directed our attention away from "chest pain" alone and physical exertion as the central provoking factor toward transient myocardial ischemia and its broader triggers and consequences. Transient myocardial ischemic episodes, the majority of which are silent, are found in a subset of patients with any clinical manifestations of CAD (eg, stable angina, unstable angina, myocardial infarction, and sudden death), as well as in those patients with CAD who are and have been totally asymptomatic. These episodes are an independent predictor of increased risk for future cardiac events. Most medical therapy and revascularization therapies have the potential to prevent or relieve these silent episodes; however, we do not yet know which method is superior in reducing SMI episodes or preventing future cardiac events. Furthermore, the benefit of reducing SMI versus the cost and potential morbidity of these chosen therapies is not known. At least three trials are now underway to examine some of these concerns (Table 2). Focus on pain relief alone does not appear to be an adequate approach to alter outcome in patients with CAD and may prove insufficient to control SMI. Until these issues are resolved, we believe a conservative approach to the management of patients with CAD is warranted. Documentation of ischemia (painful or painless) is essential. Three general principles should be kept in mind. First, the presence of detectable ischemia is of central importance. This information should be used in the overall risk assessment of the patient. Second, the level of concern or aggressiveness of treatment should be based on the risk associated with the ischemic abnormalities documented (Table 3). The exercise stress test is the most useful to begin this process. The detection of ischemic-type ST-segment depression, either silent or painful, at a low workload (eg, less than or equal to 120 beats per minute or less than or equal to 6.5 metabolic equivalents [METS]) implies high risk for adverse outcome. Likewise, these ST-segment changes occurring in leads that reflect multiple coronary artery distribution, of greater than 2 mm in magnitude and persisting for greater than 6 minutes, are all markers for high risk. Thallium redistribution defects occurring at low work loads, in multiple areas, associated with increased lung uptake and enlargement of the cardiac pool all imply high risk.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Treatment strategies for daily life silent myocardial ischemia: a correlation with potential pathogenic mechanisms. 135 7

This study examined the importance of viability as a clinical issue in 532 patients with angiographically proven CAD who underwent exercise SPECT thallium imaging. Conventional 4-hour delayed images were used to differentiate scar tissue from ischemia (20 segments per patient). There were 90 patients (17%) with normal images, 274 patients (52%) with reversible defects only, and 168 patients (31%) with scar tissue either with or without associated ischemia. The patients with scar tissue were subdivided according to the number of segments with fixed defects and the number of additional reversible defects. There were 114 patients with scar tissue alone or more scar tissue than ischemia. Contrast ventriculography in these 114 patients revealed normal wall motion or ejection fraction in 50 patients. On the basis of results of thallium imaging alone, the issue of viability was probably significant in 114 patients (21%); however, when the ventriculographic data were also included, the issue was significant in only 64 patients (12%) (p < 0.001). Thus myocardial viability is an important issue in 21% of patients with CAD when conventional thallium imaging is used, but this percentage decreases to 12% when wall motion and ejection fraction data are also included. These data may be important in considerations for the need of metabolic imaging and emerging scintigraphic techniques.
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PMID:The clinical relevance of myocardial viability in patient management. 144 3

Transient episodes of myocardial ischemia can be reliably detected by AEM in patients with known CAD. AEM appears to be particularly useful for patients in whom symptom control has been achieved with conventional antianginal drugs because many of these patients (up to 50%) continue to have residual silent ischemia that would otherwise remain undetected. Despite the lack of symptoms, numerous studies in patients with stable and unstable coronary syndromes have shown that the presence of silent ischemia during AEM is associated with an increased risk of subsequent coronary events and cardiac death. Although Holter monitoring is a practical and reliable tool for prolonged evaluation of myocardial ischemia, its routine use can not be advocated until its clinical role has been clearly defined in the ongoing large prospective studies.
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PMID:Ambulatory electrocardiography evaluation of asymptomatic, unstable, and stable coronary artery disease patients for myocardial ischemia. 150 73

Continuous ECG recording of ST segments can provide important insight into the effects of CAD in patients before, during, and after anesthesia and surgery. The stresses of anesthesia and surgery are particularly threatening to the patient with critical coronary disease and ischemia. ST-segment monitoring is a useful alternative to preoperative stress ECG in patients who are unable to exercise, particularly if radionuclide techniques are not readily available. Continuous ST-segment monitoring provides an additional and unique method of monitoring patients during and after surgery, and on-line analysis of such data provides the anesthesiologist with opportunities to recognize and promptly respond to ischemic episodes. Future studies will determine whether such aggressive strategies will alter the outcome for patients with perioperative myocardial ischemia.
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PMID:Perioperative myocardial ischemia and infarction. Detection of myocardial ischemia using continuous electrocardiography. 157 38

From January 1985 to december 1989, 83 patients (69 men, 14 women) underwent an in situ femoro-popliteal bypass using a semi-closed technique and the valvulotome developed by Dr Paul Cartier. Most patients (67%) were operated for severe ischemia while 33% were for claudication. HTA was present in 31% of patients, diabetes in 38% and CAD in 57%. Mean preoperative ABI was 0.33 +/- 0.20 and mean ankle pressure was 50 +/- 30 mm of Hg. Arteriographic popliteal run-off showed three vessels in 21 cases (25%), two vessels in 17 cases (20%) and one vessel in 38 cases (45%). Nine patients (10%) presented an isolated popliteal artery. Bypass was constructed below knee in 62 patients (73%) and above knee in 23 (27%). Five mortalities (5.8%) and two major complications (2.3%) were related to surgery. Four early graft failures (4.4%) were noted but 3 were successfully reoperated. Postoperative ABI was 0.71 +/- 0.23 mm of Hg and 81% of patients had complete relief of their symptoms. With a mean follow-up 19 months, graft patency was 91% +/- 6% and 84% +/- 11% at one and two years and was not influenced by operative indication: hypertension, diabetes, preoperative ABI, arteriographic findings or distal anastomotic site. Overall survival was 80% +/- 10% and 69 +/- 13 at one and two years. The in situ technique using the Cartier valvulotomes is an excellent operation and compares favourably with other techniques.
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PMID:[In situ femoro-popliteal bypass grafts. Study of 85 cases using Cartier's technique]. 178 15

The average annual mortality in unselected patients with chronic stable angina is 4%. Mortality is increased in male patients and in patients who have risk factors such as hypertension, previous MI, or abnormal ECGs. We do not routinely recommend cardiac catheterization in the initial management of patients with stable angina unless the patient exhibits evidence for severe myocardial ischemia on non-invasive testing or has symptoms that are refractory to treatment. In patients who undergo cardiac catheterization, the most important determinant of survival is left ventricular function followed by the number of diseased vessels. Noninvasive testing provides important additional prognostic information to cardiac catheterization data and should be used in the decision to treat a patient medically or surgically. Mortality is increased in patients who have low exercise tolerance, exercise-induced ischemia, or a poor hemodynamic response to exercise. Unstable angina in medically treated patients is associated with a 3% to 5% hospital mortality and 7% to 8% mortality in the first year. The rate of nonfatal MI is about 8% to 10% in the first 2 weeks. We routinely recommend coronary angiography unless patients have had recent cardiac catheterization or there is a major contraindication. Mortality is increased in those who fail to respond to initial therapy, who have severe left ventricular dysfunction, and who have multivessel CAD, particularly left main CAD. The question of whether all patients with unstable angina require coronary angiography for risk stratification and possible revascularization is being addressed in the TIMI III trial.
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PMID:The prognosis in stable and unstable angina. 202 4

To evaluate cardiodepressive risks of antiarrhythmic treatment with ajmaline, we monitored, in addition to conventional hemodynamic parameters, end systolic pressure-volume relations (ESPVR) to assess potential negative inotropic effects. Twelve patients (CAD without ischemia; EF = 60 +/- 3%) underwent hemodynamic analysis with and without the influence of ajmaline (1 mg/kg, i.v.) both 1) at rest (paced heart rate of 90 bpm) and 2) during tachycardia of 160 bpm. As a result, LV-pump function was found to have diminished moderately: EF by 23% vs 10%, respectively; stroke volume by 10% vs 0%; cardiac work by 5% vs 16%, and dP/dtmax by 14% vs 19%. While preload increased under the influence of ajmaline (LVEDP by 17% vs 30%), the LV-volumes increased (EDV by 18% vs 12%; ESV by 58% vs 21%), afterload remained unchanged. Ajmaline caused the loops of the ESPVR to move rightward and the slope k of the ESPVR to decrease, thus indicating loss of inotropy during the influence of the antiarrhythmic agent. Thus, ajmaline showed a tendency to generate cardiodepressive effects in patients with normal LV-function, and to depress contractility in single cases that clinically had no consequences. The conductance technique proved useful and safe in the assessment of inotropic drug effects by analyzing the ESPVR within the catheterization laboratory routine.
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PMID:[Effect of the class IA anti-arrhythmic agents ajmaline on end-systolic pressure-volume relations (conductance technique)]. 208 58


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