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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Silent ischemia is common in diabetic patients with coronary heart disease. These patients may also have more subtle alteration in the perception of angina as reflected by prolongation of anginal perceptual threshold--the time from onset of 0.1 mV ST segment depression to the onset of chest pain during treadmill exercise. Silent ischemia may be associated with a generalized hyposensitivity to pain, although the pathophysiologic mechanism is obscure. The purpose of the present study was to determine whether diabetic patients with prolonged anginal perceptual thresholds are also hyposensitive to painful stimuli and to investigate whether this is associated with autonomic neuropathy. Nineteen diabetic and 25 nondiabetic patients with exertional angina were exercised on a treadmill to measure anginal perceptual threshold. Somatic pain threshold was measured by calf sphygmomanometry. The cuff was inflated rapidly until pain occurred, and six repeat inflations were done to test reproducibility. Because there was no significant difference between measurements (coefficient of variation = 0.156) the mean value for each patient provided a measure of somatic pain threshold. The diabetic group had a longer anginal perceptual threshold (138 +/- 64 seconds vs 34 +/- 51 seconds, p less than 0.001), which correlated positively with the somatic pain threshold (r = 0.5, p = 0.03); patients with more prolonged anginal perceptual thresholds tended to have higher somatic pain thresholds. In the diabetic group anginal perceptual (r = -0.3, p = NS) and somatic pain (r = -0.4, p = 0.05) thresholds tended to increase as the ratio of peak to minimal heart rate during the Valsalva maneuver fell below 1.21, but these variables were unrelated in the nondiabetic group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The perception of angina in diabetes: relation to somatic pain threshold and autonomic function. 159 62

We studied the effect of propranolol administration on risk assessment based on submaximal exercise testing performed early after myocardial infarction. A total of 70 patients with recent infarction underwent modified Bruce treadmill testing with simultaneous measurement of expired gases in the absence of antianginal agents including beta-antagonists. Among these, 31 patients who had at least one of the following abnormalities--ST depression greater than or equal to 1 mm (22 patients), chest pain (four patients), or treadmill time less than 360 seconds (12 patients)--were studied in a randomized double-blind fashion and received either placebo or 240 mg of propranolol/day. A total of 28 patients completed the randomized phase and were able to undergo repeat exercise testing an average of 3.4 +/- 1.8 days later. Randomized groups were equivalent at baseline except for a higher peak oxygen consumption and carbon dioxide production (p less than 0.05) in the propranolol compared with the placebo group; these differences were taken into account in statistical analyses of the study data. Resting heart rate (59 +/- 1.2 versus 82 +/- 4.2 beats/min) and peak heart rate x systolic blood pressure (14,208 +/- 496 versus 20,075 +/- 1,062) were both significantly less (p less than 0.01) after propranolol than after placebo. Eight of nine patients treated with placebo maintained ST depression greater than or equal to 1 mm from the initial to the randomized exercise test, compared with only 4 of 13 receiving propranolol (p less than 0.01). In those with continued ST depression, time to positivity was significantly longer in those receiving propranolol compared with those taking placebo (538 +/- 73 versus 318 +/- 44 seconds, p less than 0.05). In contrast, the peak ratio between carbon dioxide production and oxygen consumption was higher in those receiving propranolol compared with those receiving placebo (0.93 +/- 0.04 versus 0.81 +/- 0.03, p less than 0.05). We conclude that propranolol therapy reduces evidence of ischemia and changes traditional estimates of potential cardiac risk derived from submaximal postinfarction exercise testing.
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PMID:Propranolol therapy alters estimation of potential cardiovascular risk derived from submaximal postinfarction exercise testing. 203 80

The possibility that myocardial ischemia may be associated with chest pain during painful crises was evaluated prospectively in 20 patients (11 women and nine men) with sickle cell disease (19 SS, 1 S beta + thalassemia). Sixteen of 20 (80%) had abnormal ECGs, 7 (35%) had transient ST-T wave changes, and 3 (15%) had persistent ST-T wave changes, both consistent with ischemia; 6 (30%) had nonspecific ST-T changes, and 4 (20%) had normal tracings. Serum enzymes (CK, SGOT, LDH) were abnormal in 16 of 19 (84%); 1 had CK-MB detected, (5%) and 1 had LDH1 to LDH2 reversal. All 10 Tc-99m pyrophosphate scans performed were negative; 4 of 6 (66%) thallium-201 scans had focal defects, and 5 of 8 (63%) radionuclide angiograms (MUGAs) had focal wall motion abnormalities. Three of 8 (38%) MUGAs showed cardiac dilation, diffuse hypokinesis, and reduced ejection fractions. Thus, myocardial damage may be a potentially serious complication of patients with sickle cell anemia who present with chest pain during painful crises. Studies are indicated to define the significance and pathophysiology of these observations.
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PMID:Sickle cell anemia: does myocardial ischemia occur during crisis? 203 80

Bypass graft stenosis and occlusion are relatively common events, occurring eventually in the majority of patients who survive beyond 5 years after coronary artery bypass graft surgery. These processes, in combination with progressive native coronary artery disease, lead to recurrent angina and an increased need for medication in most patients late after surgery. Patients with unstable ischemic symptoms generally should proceed directly to coronary arteriography, whereas patients with stable angina may be candidates for noninvasive testing to evaluate their risk and the extent of myocardial jeopardy. If the initial revascularization procedure is successful, preoperative thallium 201 imaging abnormalities should be reversed. Persistent abnormalities beyond 6 months after revascularization indicate incomplete revascularization or perioperative infarction. Defects noted in the immediate postoperative period may be areas of myocardial stunning or hibernation, which can require up to 6 months to reverse. If chest pain recurs after revascularization, a normal thallium 201 perfusion pattern indicates that the symptom is probably not ischemic in nature. Thallium 201 perfusion abnormalities may precede symptoms by several months and may be the only indication of significant myocardial ischemia in patients with silent ischemia. Advanced tomographic imaging techniques, such as single photon emission computed tomography (SPECT), should theoretically improve disease detection and localization following revascularization. Practically speaking, only the left anterior descending coronary bed is well evaluated by these tomographic imaging techniques. The sensitivity and specificity of SPECT imaging for evaluation of posterior circulation abnormalities remains unacceptably low. Complexities of competitive flow and collateralization that may exist in the postoperative period make it difficult to relate perfusion abnormalities to a specific graft stenosis. However, tomographic perfusion imaging may provide useful correlative information on the functional impact of bypass graft stenoses in patients with recurrent angina who have undergone coronary angiography and in whom the angiographic indications for repeat surgery or angioplasty are not compelling. Newer tomographic and metabolic imaging techniques such as CT, NMRI, and PET remain unproven as diagnostic tests for the evaluation of unselected patient populations presenting with recurrent angina following revascularization surgery.
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PMID:Evaluation of the patient with stable angina following coronary artery bypass surgery. 204 87

To assess the reliability of the exercise ECG in detecting silent ischemia, ECG results were compared with those of stress-redistribution thallium-201 single-photon emission computed tomography (SPECT) in 116 patients with prior myocardial infarction and in 20 normal subjects used as a control. The LV was divided into 20 segmental images, which were scored blindly on a 5-point scale. The redistribution score was defined as thallium defect score of exercise subtracted by that of redistribution image and was used as a measure of amount of ischemic but viable myocardium. The upper limit of normal redistribution score (= 4.32) was defined as mean +2 standard deviations derived from 20 normal subjects. Of 116 patients, 47 had the redistribution score above the normal range. Twenty-five (53%) of the 47 patients showed positive ECG response. Fourteen (20%) of the 69 patients, who had the normal redistribution score, showed positive ECG response. Thus, the ECG response had a sensitivity of 53% and a specificity of 80% in detecting transient ischemia. Furthermore, the 116 patients were subdivided into 4 groups according to the presence or absence of chest pain and ECG change during exercise. Fourteen patients showed both chest pain and ECG change and all these patients had the redistribution score above the normal range. Twenty-five patients showed ECG change without chest pain and 11 (44%) of the 25 patients had the abnormal redistribution. Three (43%) of 7 patients who showed chest pain without ECG change had the abnormal redistribution score. Of 70 patients who had neither chest pain nor ECG change, 19 (27%) had the redistribution score above the normal range. Thus, limitations exist in detecting silent ischemia by ECG in patients with a prior myocardial infarction, because the ECG response to the exercise test may have a low degree of sensitivity and a high degree of false positive and false negative results in detecting silent ischemia.
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PMID:[Reliability of the exercise ECG in detecting silent ischemia in patients with prior myocardial infarction]. 204 81

Atrial repolarization waves are opposite in direction to P waves, may have a magnitude of 100 to 200 mu V and may extend into the ST segment and T wave. It was postulated that exaggerated atrial repolarization waves during exercise could produce ST segment depression mimicking myocardial ischemia. The P waves, PR segments and ST segments were studied in leads II, III, aVF and V4 to V6 in 69 patients whose exercise electrocardiogram (ECG) suggested ischemia (100 mu V horizontal or 150 mu V upsloping ST depression 80 ms after the J point). All had a normal ECG at rest. The exercise test in 25 patients (52% male, mean age 53 years) was deemed false positive because of normal coronary arteriograms and left ventricular function (5 patients) or normal stress single photon emission computed tomographic thallium or gated blood pool scans (16 patients), or both (4 patients). Forty-four patients with a similar age and gender distribution, anginal chest pain and at least one coronary stenosis greater than or equal to 80% served as a true positive control group. The false positive group was characterized by 1) markedly downsloping PR segments at peak exercise, 2) longer exercise time and more rapid peak exercise heart rate than those of the true positive group, and 3) absence of exercise-induced chest pain. The false positive group also displayed significantly greater absolute P wave amplitudes at peak exercise and greater augmentation of P wave amplitude by exercise in all six ECG leads than were observed in the true positive group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Identification of false positive exercise tests with use of electrocardiographic criteria: a possible role for atrial repolarization waves. 205 Sep 16

Myocardial ischemia must be the first concern of every emergency physician in evaluating chest pain in the adult patient. Any suspicion of myocardial ischemia must be promptly evaluated and admitted. The American College of Emergency Physicians has recently published a standards document on the care of chest pain in the adult patient. The emergency physician must be familiar with this document. Once myocardial ischemia and other life-threatening causes are ruled out, one can consider that cervical disk disease may be the cause of chest pain. We present two cases of patients who presented to the emergency department with signs and symptoms consistent with cardiac ischemia. Both patients were found to have herniated cervical disks. Subsequent surgical repair completely relieved their symptoms. Evaluation of the literature shows that this entity was well described from 1950 to the 1960s. Most recent discussions do not mention disk herniation as even an infrequent cause of chest pain. If there is no life-threatening disease present, one should consider cervical disk disease.
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PMID:Herniated cervical disk presenting as ischemic chest pain. 205 5

Repeated episodes of myocardial ischemia might lead to progressive impairment of left ventricular (LV) function. This radionuclide study assessed myocardial ischemia and LV function several years after documented coronary occlusion without myocardial infarction. Over 5 years, 24 consecutive patients, who underwent cardiac catheterization for angina pectoris without myocardial infarction, had isolated total occlusion of the left anterior descending coronary artery with well-developed collateral vessels. Five patients were successfully treated by coronary bypass grafting and 3 by coronary angioplasty. Among the 16 medically treated patients, 1 was lost to follow-up and 1 died (extracardiac death). The mean (+/- standard deviation) follow-up (14 patients) was 48 +/- 15 months. At follow-up, 8 patients still had clinical chest pain, 11 received antianginal therapy, 4 patients had no stress ischemia and the other 10 had greater than or equal to 1 sign of stress ischemia. All patients had a normal LV ejection fraction at rest (mean 60 +/- 3%; range 55 to 65%). Collateral circulation preserves LV function at the time of occlusion and, in some cases, prevents the development of myocardial ischemia; in patients with persisting myocardial ischemia after well-collateralized coronary occlusion, LV function is not impaired at long-term follow-up.
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PMID:Evolution of myocardial ischemia and left ventricular function in patients with angina pectoris without myocardial infarction and total occlusion of the left anterior descending coronary artery and collaterals from other coronary arteries. 205 62

Dipyridamole thallium-201 scintigraphy (DP-Tl) and coronary angiography were studied on 74 patients with suspected coronary artery disease. We compared the clinical features, hemodynamic responses, angiographic results and scintigraphic findings of patients who had chest pain during DP-Tl testing ('chest pain' group) with those of patients who did not have chest pain ('no pain' group). Thirty eight (51%) of the 74 patients developed chest pain. Heart rate and rate pressure product during DP infusion of 'chest pain' group were greater than those of the 'no pain' group (p less than 0.05). Ischemic ST depression was more frequently observed among 'chest pain' patients (p less than 0.01). There were no differences in angiographic severity of coronary artery disease between 'chest pain' and 'no pain' group. Also, we could find no differences in extent and severity scores of perfusion defects and washout abnormalities between the two groups. However, when patients with myocardial infarction were excluded, the 'chest pain' group had significantly greater extent and severity scores of washout abnormalities than the 'no pain' group (extent score: 38 +/- 8 vs 18 +/- 5, p less than 0.05, severity score: 55 +/- 15 vs 18 +/- 7, p less than 0.01). Our study indicated that in patients without myocardial infarction, patients with 'chest pain' had more severe ischemia than 'no pain' patients. But in patients with myocardial infarction, myocardial ischemia not accompanied by chest pain might be as severe as that with chest pain. The presence or absence of myocardial infarction might have great influence on results regarding the relation of chest pain to myocardial ischemia.
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PMID:The relationship between chest pain during thallium-201 scintigraphy with dipyridamole and myocardial ischemia. 206 96

The possibility of early prediction of acute myocardial infarction (AMI) was assessed in 7,157 consecutive patients coming to our emergency room during a 21-month period with chest pain or other symptoms suggestive of AMI. Of these patients 921 developed an AMI during the first 3 days in the hospital. Of the 4,690 patients admitted to hospital, 1,576 (34%) had a normal admission electrocardiogram, and 90 of these (6%) developed AMI. Of 1,964 patients with an abnormal electrocardiogram without signs of acute ischemia (42% of those admitted), 268 (14%) developed AMI, and 563 (51%) of 1,109 patients with acute ischemia on the electrocardiogram (24%) developed AMI. All patients were prospectively classified in the emergency room on the basis of history, clinical examination and electrocardiogram into 1 of 4 categories, according to the initial degree of suspicion of AMI. Of 279 admitted patients judged to have an obvious AMI (6% of the 4,690), 245 (88%) actually developed AMI; of 1,426 with a strong suspicion of AMI (30%), 478 (34%) developed one; of 2,519 with a vague suspicion of AMI (54%), 192 (8%) developed one; and of 466 with no suspicion of AMI (10%), 6 (1%) developed one. Thus, only a low percentage of the patients with a normal initial electrocardiogram or a vague initial suspicion of AMI developed a confirmed AMI.
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PMID:Early prediction of acute myocardial infarction from clinical history, examination and electrocardiogram in the emergency room. 206 77


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