The return of silent ischaemia? Not really.
Patients with a positive but asymptomatic test for the detection of underlying ischaemia should be treated with the same commitment as those with a similar but symptomatic test.
Coronary Angiography↗
Biomedical subjects
D A Mulcahy
Publications and source records attributed to D A Mulcahy.
Why is recurrent myocardial ischaemia a predictor of adverse outcome in unstable angina? An observational study of myocardial ischaemia and its relation to coronary anatomy.
OBJECTIVE: To establish why recurrent myocardial ischaemia predicts adverse outcome in patients with refractory unstable angina on maximal medical treatment. DESIGN: Prospective observational study in 101 patients with refractory unstable angina who underwent continuous ST-segment monitoring and kept detailed pain charts prior to cardiac catheterization. Setting Tertiary referral centre. RESULTS: Significant coronary disease was identified in 90 subjects with 74 (82%) having multivessel disease, 41 (46%) complex lesion morphology, and 10 (11%) subjects with definite features of intra-coronary thrombus. The frequency of complex lesions or intra-coronary thrombus did not differ in relation to the extent of coronary disease. Recurrent chest pain was present in 72 of the 90 (80%) subjects, while transient ischaemia was detected in 26 (29%). The presence of transient ischaemia was a powerful predictor of complex lesions or thrombus (odds ratio 7.1;P<0.001). Subjects with severe recurrent chest pain had a greater frequency of intracoronary thrombus (odds ratio 9.5;P<0.05). CONCLUSIONS: In unstable angina once the normal mechanisms causing myocardial ischaemia (i.e. increased myocardial demand and coronary vasoconstriction) have been treated using maximal antianginal treatment, the continued development of transient myocardial ischaemia is strongly associated with complex coronary lesion morphology and intracoronary thrombus. It is already known that patients with complex lesion morphology and intracoronary thrombus have an adverse outcome in unstable angina and therefore it is this association that explains why transient ischaemia is a predictor of poor outcome in unstable angina.
Adult↗
Genes, greens, and homocysteine.
Explore the source record for details and available documents.
Angina Pectoris↗
Percutaneous transluminal coronary angioplasty in chronic coronary artery occlusion.
OBJECTIVES: This study was conducted to determine the procedural success rate, complication rate and long-term outcome of percutaneous transluminal coronary angioplasty in chronically occluded coronary arteries. BACKGROUND: Coronary angioplasty of chronically occluded vessels has a lower success rate than has angioplasty of nonoccluded vessels, but it is frequently considered safe because the target vessel is already occluded. The purpose of this study was to determine the reliability of these assumptions at our institution, with the objectives stated above. METHODS: We identified from the angioplasty data base at our institution 100 consecutive coronary angioplasty procedures performed between 1987 and 1991 for chronic total occlusion, defined as complete occlusion (Thrombolysis in Myocardial Infarction [TIMI] grades 0 and 1 flow) for > or = 3 months. The records of the 95 patients who underwent these procedures were reviewed to determine procedural outcome and medium-term results. RESULTS: Procedural success was obtained in 47 occluded vessels (47%). Significantly fewer successes were obtained in the right coronary artery (26.8%) than in either the left anterior descending (57.1%) or the left circumflex (45%) coronary artery (p < 0.05). A procedural failure without serious adverse consequences occurred in 45 procedures (45%), but in eight patients (right coronary artery in five, left anterior descending artery in three) attempted recanalization was complicated by extensive coronary dissection with acute myocardial ischemia, and one of these patients died. There were no emergency operations, but elective coronary artery bypass surgery was undertaken in 26 patients (in 3 after extensive dissection, in 7 after an apparently good result and in 16 in whom the procedure failed). At 12 months after the procedure, 64.1% of those with a procedural success were event free compared with 32.6% of those whose procedure was both unsuccessful and uncomplicated (p < 0.025) and 25% of those in whom it was unsuccessful and complicated by coronary dissection (p < 0.025). CONCLUSIONS: In this series of recanalization of chronically occluded coronary arteries, there was a low procedural success rate, particularly for the right coronary artery. However, when procedural success was obtained, the long-term outlook was good. The overall risk of coronary dissection was comparable to the risk in nonoccluded vessels but was particularly high in the right coronary artery (13%).
Adult↗
Circadian rhythms in cardiovascular function.
This short overview discusses circadian rhythms observed in cardiovascular events such as myocardial ischaemia and myocardial infarction, which occur most frequently in the morning. Changes in the frequency of occurrence seem to be related to, and may result from, circadian rhythms in factors such as heart rate, blood pressure, coronary artery tone, platelet adhesiveness and blood fibrinolytic activity, which could be involved in triggering myocardial ischaemia or infarction. Consideration of the circadian rhythm of myocardial ischaemia and serious cardiovascular events may be important when medical therapy is selected.
Circadian Rhythm↗
Circadian variation of the total ischemic burden and influence by beta-blocking agents.
We investigated 150 unselected patients with proven coronary artery disease. All patients were off all routine antianginal treatments and there were 598 ischemic episodes, of which 75% were silent. It was found that episodes of ischemia, both silent and painful, occurred predominantly during the daytime hours from 0730 to 1930 h. This pattern is similar to that described by others. There was a significant excess of episodes of ischemia in the morning hours (0730-1330 h), with a secondary peak occurring in the evening hours. We further investigated a subgroup of 41 patients who were monitored for 1,581 h while being treated with atenolol. These patients were investigated in a double-blind fashion, and during the off treatment phase the circadian pattern of ischemic episodes was similar to that described for the group as a whole. However, on treatment with atenolol, there was a significant reduction in the frequency and total duration of ischemic episodes throughout the day. Atenolol significantly altered the circadian distribution of ischemic episodes with elimination of the morning peak; there was some preservation of the evening peak although this was smaller than that described when the patients were off therapy. The circadian distribution of ischemic episodes and the observed changes with beta-blocking treatment resemble the reported circadian variation of acute myocardial infarction and sudden death. Although these studies do not in any way prove that myocardial ischemic episodes and their alteration by treatment are related to the development of acute myocardial infarction and death, the relationship between ischemic episodes and the end points of coronary disease require further investigation.
Adrenergic beta-Antagonists↗
Therapeutic rationale for the management of silent ischemia.
Prognostic data on the importance of silent ischemia is lacking. Preliminary reports suggest that ambulatory electrocardiographic monitoring provides additional information not contained in the exercise test, but it is still unclear whether silent ischemia is a marker of subsequent events or is responsible for their development. Recent investigations also suggest that intermittent episodes of ischemia may cause myocardial necrosis. Drugs that are effective in the treatment of angina are also effective in the treatment of silent ischemia, but their value in terms of long-term morbidity and mortality is unclear. Recently, the circadian distribution of silent ischemia has been reported in 150 patients off therapy, in 33 receiving nifedipine, and in 41 receiving atenolol. Most ischemic episodes off therapy occurred between 7:30 AM and 7:30 PM with a peak in the morning and a lesser peak in the evening. Nifedipine did not alter the circadian pattern of ischemic episodes; atenolol abolished the morning peak, the peak incidence of ischemia then occurring in the evening. This circadian distribution of ischemic episodes and the observed changes with treatment resemble the reported circadian variations of acute myocardial infarction and sudden death. Large multicenter studies are now being performed to determine the effects of treatment on silent ischemia and how this treatment may influence outcome. Until such studies have been completed, it is not possible to clearly define the indication for drug therapy in the management of silent ischemia.
Circadian Rhythm↗