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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve different approaches to laboratory diagnosis of angina pectoris are reviewed here. They employ no fewer than seven different means of intentionally provoking a disparity between myocardial requirement and supply: dynamic exercise, hypoxia, prandial stress, raised systemic vascular resistance, paced tachycardia, mental stress, and exposure to normal environment. Of these, only dynamic exercise and the diverse combinations of stresses in the normal environment are capable of altering the heart's oxygen requirement-supply ratio threefold or more, accounting for the successful results from tests using these means of stress. The reviewed tests use three different means of detecting myocardial ischemia provoked by stress: electrocardiography to indicate impaired ventricular repolarization, indirect graphic records sensitive to impairment of mechanical ventricular function, and detection of insufficient myocardial perfusion patterns by radioactive tracer. The latter approach is particularly appealing because it directly reflects the pathophysiologic anomaly of interest. It should be remembered, however, that the basic differences in these methods of detecting ischemia make them complementary to each other and encourage their use in combination for improved diagnostic sensitivity.
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PMID:Interesting approaches to the diagnosis of angina pectoris. 63 19

In patients with coronary artery disease, radionuclide investigations have documented a high incidence of mental stress-induced myocardial ischemia in the absence of significant electrocardiographic changes and/or angina. To investigate the causes of the low electrocardiographic sensitivity, we recorded body surface maps during mental arithmetic in 22 normal volunteers and 37 postinfarction patients with residual exercise ischemia. Myocardial perfusion was studied with thallium-201 or technetium-99 (SESTAMIBI) planar scans. In 14 patients, body surface maps were also recorded during atrial pacing at the heart rate values achieved during mental stress. While taking the body surface maps, the area from J point to 80 msec after this point (ST-80) was analyzed by integral maps, difference maps, and departure maps (the difference between each patient's difference map and the mean difference map for normal subjects). The body surface mapping criteria for ischemia were a new negative area on the integral maps, a negative potential of more than 2 SD from mean normal values on the difference maps, and a negative departure index of more than 2. Scintigraphy showed asymptomatic myocardial hypoperfusion in 33 patients. Eight patients had significant ST segment depression. The ST-80 integral and difference maps identified 17 ischemic patients. Twenty-four patients presented abnormal departure maps. One patient presented ST depression and abnormal body surface maps without reversible tracer defect. In 14 of 14 patients, atrial pacing did not reproduce the body surface map abnormalities. The analyses of the other electrocardiographic variables showed that in patients with mental stress-induced perfusion defects, only changes of T apex-T offset (aT-eT) interval in Frank leads and changes of maximum negative potential value of aT-eT integral maps significantly differed from those of normal subjects. Our results confirm the low electrocardiographic sensitivity for detecting mental stress-induced myocardial hypoperfusion in postinfarction patients. ST analysis in the body surface map increases the information content of the electrocardiographic signal. T wave analysis appears to offer fewer diagnostic advantages.
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PMID:Electrocardiographic markers of ischemia during mental stress testing in postinfarction patients. Role of body surface mapping. 182 36

In asymptomatic patients the importance of silent ischemic ST-T wave changes on Holter monitoring is known to be a significant predictive variable for one-year mortality of postmyocardial infarction patients. This case report represents the uses of ambulatory ECG to detect ischemic ST changes in patients who have had recent strokes. The cases reported here of silent myocardiac ischemia in stroke patients reflect previous reports in which 70% of the ischemic episodes in patients with symptomatic coronary artery disease are not associated with angina and in which approximately 10% to 15% of acute myocardial infarctions are silent. We now believe that the incidence of "silent" ischemia may be precipitated in poststroke patients during their rehabilitation program. This belief is supported by two main factors. First, a high level of personally relevant mental stress exists which activates the sympathoadrenal system, which may lead to myocardial ischemia. Second, some stroke patients become aphasic and are unable to communicate adequately even if they experience angina symptoms. We have found that poststroke, most patients could not undergo exercise treadmill testing secondary to a variety of factors: inability to coordinate limbs, poor endurance, inability to follow directions, and/or lack of attention. We now propose that 24-hour monitoring for ST-T wave changes poststroke should be considered as part of a vigorous investigation for myocardial ischemia during the rehabilitation of these patients because they have an increased risk of cardiac morbidity.
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PMID:Silent myocardial ischemia during rehabilitation for cerebrovascular disease. 198 25

To assess the prevalence of mental stress-induced myocardial ischemia and investigate the pathogenetic mechanisms by which emotional stress may induce myocardial ischemia, we studied 372 patients with angina pectoris who underwent mental arithmetic and exercise stress testings. Hyperventilation tests were also performed in 176 patients, and 340 patients underwent coronary arteriography. Sixty-one patients showed significant ST segment abnormalities during mental arithmetic and exercise stress testings (group 1). Two hundred eleven patients had negative responses to mental stress but positive exercise tests (group 2), whereas both tests were negative in 100 patients (group 3). Mental stress induced significant increases in heart rate and systolic blood pressure in the three groups of patients; however, group 1 patients had higher increases in rate-pressure product (mm Hg x beats/min) than group 2 and group 3 patients (14,909 +/- 3,894 versus 12,985 +/- 2,900 versus 12,724 +/- 4,400 mm Hg x beats/min, p less than 0.01). Group 1 patients had shorter exercise durations than group 2 or group 3 (4.06 +/- 1.55 versus 7.65 +/- 3.07 versus 13.9 +/- 5.31 minutes, p less than 0.01), although rate-pressure products at peak exercise were similar in groups 1 and 2 (20,277 +/- 6,058 versus 20,768 +/- 3,864, p = NS) and significantly higher in group 3 (26,221 +/- 7,100/mm Hg x beats/min, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mental stress as a provocative test in patients with various clinical syndromes of coronary heart disease. 200 19

Incidence and mechanisms of psychological stress-induced myocardial ischemia were investigated in a population of 63 patients using mental arithmetic. Fifty subjects (group 1) were selected as a consecutive population of ischemic patients with electrocardiographic documentation of ischemia at rest, on effort, or both. Mental arithmetic induced increases in heart rate, blood pressure, and rate-pressure product in all patients. Transient ischemic electrocardiographic changes occurred in 22 patients (44%; positive mental arithmetic), the majority of whom had both resting and exercise angina. In negative mental arithmetic tests, peak rate-pressure product was always lower than that achieved during exercise (mean +/- SD, 11.9 +/- 3 versus 21.3 +/- 5, p less than 0.01). Of the 22 patients with positive mental arithmetic tests, ischemia occurred in only six, at a rate-pressure product equal to or more than the one achieved during exercise (21.1 +/- 5 versus 19.4 +/- 4, p less than 0.01), suggesting an increase in myocardial O2 demand exceeding the limited increase in flow; in the remaining 16 patients, rate-pressure product values were significantly lower (14.8 +/- 3 versus 22.7 +/- 6, p less than 0.01), suggesting a primary reduction in coronary blood flow that is probably related to an increase in coronary tone. To assess the possible site of such a vasoconstriction, the effect of mental arithmetic on large coronary artery diameter was tested in 13 additional unselected patients (group 2) undergoing coronary angiography for a chest pain syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary dynamics and mental arithmetic stress in humans. 200 34

Ventricular arrhythmias detected in the late-hospital phase of myocardial infarction have been identified as a risk factor for sudden death, being their prognostic value independent of ventricular function. However, relations between both factors are not clarified. In order to study hypothetic associations between ventricular arrhythmias and some clinical, hemodynamic and angiographic variables, 60 patients (52 males, 8 females) underwent 24-hour Holter recordings and cardiac catheterization with left ventricular and coronary angiographies, 3-5 weeks after hospital admission. Past history data, acute phase complications and hemodynamic and angiographic results were compared between patients with and without significant ventricular arrhythmias during Holter monitoring (10 or more PVC's/hour and/or repetitive forms). No significant differences were found between both groups neither in mean age nor in the incidence of previous angina or infarction, cerebral ischemia, diabetes, lipid disorders or subjective feeling of being under psychological stress. Prior history of arterial hypertension was, however, significantly more frequent in patients with ventricular arrhythmias (53.3% vs 17.8%; p = 0.0183). No differences were observed in the localization of the infarct or in the complications during the acute phase (CPK peak, Killip's score, angina after 24 hours of evolution, intraventricular or A-V conduction disorders and supraventricular and ventricular arrhythmias). Among hemodynamic data, only left ventricular and aortic systolic pressures were different in both groups, being significantly higher in patients with ventricular arrhythmias. There were not differences in left ventricular segmentary contraction and in number of coronary vessels involved. To conclude, significant ventricular arrhythmias were recorded in 25% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anatomo-functional substrate of high risk arrhythmia after myocardial infarct]. 239 9

Eighteen patients, five women and 13 men, (mean age 70 +/- S.E.M. 2 years) treated with QT sensing rate responsive pacemakers due to symptomatic high degree AV block took part in a double-blind study, comparing the rate responsive (TX) mode with fixed rate ventricular inhibited (VVI) pacing. The pacemaker was blindly programmed to either mode in a cross-over design. During the 1 month period a daily diary of symptoms (chest pain, vertigo, dyspnea, and palpitations) was kept. At the end of each period, a mental stress test and an exercise test were performed. The patient rated the general well-being and stated a preference for one of the modes. In the TX mode the heart rate was significantly higher at the end of exercise compared with VVI (107 +/- 4 vs 73 +/- 3 bpm; P less than 0.001) and the exercise tolerance was improved by 9% (104 +/- 8 vs 96 +/- 7 W; P less than 0.01). The patients reported significantly less dyspnea and fatigue at comparable workloads with TX pacing. During the mental stress test the pacing rate increased by 10% in the TX mode (from 73 +/- 2 to 82 +/- 4 bpm; P less than 0.001). There was a physiological rate variability on 24-hour Holter monitoring. Ten patients reported a significant improvement in feeling of general well-being in the TX mode. Eleven patients preferred the TX mode, five patients could not distinguish between the modes and two patients preferred the VVI mode due to worsening of angina pectoris with TX pacing. This preference for the TX mode was significant (P less than 0.05). The results of this controlled study indicate that TX is preferable to VVI in most cases, but the worsening of angina pectoris in two of the patients and the occurrence of rapid rate oscillations in a third patient are factors that warrant some caution in selecting patients.
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PMID:QT sensing rate responsive pacing compared to fixed rate ventricular inhibited pacing: a controlled clinical study. 246 48

The current study was designed to examine cardiovascular reactivity to psychological tasks and its relationship to provocation of ischemia in asymptomatic coronary artery disease (CAD) patients with documented silent ischemia and those with painful ischemia. ECG, heart rate, and blood pressure responses to mental stress were collected for 13 patients with coronary artery disease (CAD) and for 6 healthy control subjects. Six of the CAD patients were asymptomatic (documented silent ischemia and no history of angina), while the remaining 7 were symptomatic (history of angina). Three types of mental stress were employed: white noise (a passive stressor), digits repeated backwards (an active stressor), and a math task plus white noise (active + passive stressor). Results indicate that significant increases in heart rate and blood pressure, but not silent ischemic episodes, were induced by the mental stress tasks. In addition, patients with documented exercise-induced and ambulant silent ischemia showed trends of blunted autonomic responsiveness to the stressors. On the digits backwards task, the CAD patients with silent ischemia showed significantly lower diastolic blood pressure responses compared with controls or angina patients. Findings suggest that ischemic episodes are not easily induced by brief mental stress. However, results indicate that asymptomatic CAD patients with silent ischemia may be lacking in autonomic responsiveness, particularly in terms of peripheral resistance, to mental stress in comparison with health controls and symptomatic ischemic patients. Further investigation is needed to explore how patients with silent ischemia typically respond autonomically to mental stress and how blunted reactivity may relate to the provocation of unrecognized ischemic episodes.
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PMID:Cardiovascular reactivity and silent ischemia in response to mental stress in symptomatic and asymptomatic coronary artery disease patients: results of a pilot study. 258 55

Myocardial ischemia is an imbalance between consumption and production of adenosine triphosphate (ATP) that leads to ATP depletion and a cascade of biochemical events. Why some patients have pain during these events while others do not is unclear, but some studies indicate that a combination of pain threshold and magnitude of ischemia may be at work. Ischemia can occur during vigorous or daily activities or at rest and can be influenced by mental stress. It is most common in the morning hours, possibly because heart rate, blood pressure, and contractility rise rapidly in the morning and factors that increase coronary vessel tone and reduce blood flow also increase during these hours. The specific pathophysiology of an ischemic episode depends on whether the patient also has chronic stable coronary disease, variant angina, or unstable angina, not on whether the episode is silent or symptomatic.
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PMID:What causes silent myocardial ischemia? 281 27

Coronary heart disease has many different clinical courses: it can cause rhythm-disturbances, sudden death, pump-failure, no pain at all (silent ischemia) or typical angina. Heart-pain can occur "on demand" after physical or mental stress with a duration of 3 to 5 minutes with typical location and good response to nitrates. It also can cause atypical forms of angina such as angina on rest, mostly due to coronary spasms. Angina can stable over months and years but can suddenly increase in severity and duration. This form is called unstable angina, which has to be recognized as soon as possible since acute myocardial infarctions evolve rather frequently. Infarction is an irreversible myocardial damage but before it develops many measures can be taken to preserve the jeopardized myocardium. The recognition and differentiation of angina pectoris is therefore of utmost importance.
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PMID:[Angina pectoris]. 305 92


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