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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To identify the effect of myocardial ischemia on systemic neurohormones and vascular resistance, 32 untreated, normotensive patients with coronary artery disease underwent incremental atrial pacing until angina. Arterial and coronary venous lactate and arterial values of catecholamines and angiotensin II were determined at control, at maximal pacing rates, and at 1, 2, 5 and 30 minutes after pacing. Based on pacing-induced ST-segment depression (greater than or equal to 0.1 mV) or myocardial lactate production, or both, patients were selected as ischemic (n = 25) or nonischemic (n = 7). Baseline clinical and hemodynamic data were comparable. During pacing, chest pain was similar (20 ischemic vs 7 nonischemic patients). Also, hemodynamic measurements were comparable, except for contractility, which did not improve, and left ventricular end-diastolic pressure, which significantly increased in ischemic patients. Moreover, during ischemia arterial pressures increased significantly (13%) and systemic resistance increased from 1,470 +/- 60 (control) to 1,632 +/- 76 dynes.s.cm-5 5 minutes after pacing (p less than 0.05) in ischemic but not in nonischemic patients. Pacing did not affect neurohormones in nonischemic patients. In contrast, norepinephrine in ischemic patients increased significantly from 1.7 +/- 0.2 (control) to 2.6 +/- 0.3 (maximal pacing) and to 3.0 +/- 0.4 nmol/liter (1 minute after pacing), whereas angiotensin II levels increased from 6.2 +/- 1.4 (control) to 9.3 +/- 2.1 pmol/liter (1 minute after pacing, p less than 0.05). Epinephrine only increased during maximal rates (0.9 +/- 0.1 vs 0.6 +/- 0.1 nmol/liter at control, p less than 0.05). Thus, myocardial ischemia activates circulating catecholamines and angiotensin II, accompanied by systemic vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Systemic neurohumoral activation and vasoconstriction during pacing-induced acute myocardial ischemia in patients with stable angina pectoris. 206 79

Angina-like chest pain, caused by alterations of esophageal function, is an increasingly common occurrence confronting cardiologists: advances in pathogenetic knowledge and in diagnostic possibilities in this field have in fact shed light on the prevalence of esophageal angina, which is present in approximately 60% of patients with angiographically intact coronaries (11% of anginal patients overall). Classically, esophageal chest pain is attributed to alterations of motility or to mucosal disease (pathologic gastro-esophageal reflux of the acid, mixed or alkaline type): this last cause prevails quantitatively. Little is known of the nociceptive mechanisms triggered by these alterations: as far as mucous disease is concerned, activation of the chemosensitive receptors has been postulated, while esophageal mechanoreceptors may be activated, in the course of a motor disorder, by distension of the wall. A recently proposed additional mechanism consists in the induction of parietal esophageal ischemia by chemical or mechanical injury: it is a fascinating and potentially resolvable mechanism, which however requires further investigation. Moreover, elements of psychological nature are also involved in the genesis of esophageal pain. A diagnosis of esophageal angina, heavily conditioned by obvious considerations of prognostic order, must necessarily aim for "certainty". Prolonged monitoring of the endoluminal pH and the adoption of provocative tests, in the course of pH monitoring and manometry, play an important role in achieving this aim (ergometric test, distension induced with a balloon, edrophonium, electrostimulation, seem most effective). A promising outlook is supported by the recent introduction of prolonged manometry. Finally, diagnostic attitude must necessarily abandon its limited specialistic horizon to consider the patient's profile in its entirety.
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PMID:[Esophageal angina]. 206 70

Rapid reduction of blood pressure by vasodilators in severe hypertensives has been associated with T-wave inversion. The significance of these changes in the absence of chest pain or other manifestations of ischemia is not known. To determine if these T-wave inversions are due to myocardial ischemia, we obtained electrocardiograms and left ventricular wall motion studies (2-D echocardiography) before and 1 h after rapid blood pressure reduction with nifedipine in 23 severe hypertensives. One hour after 10 mg nifedipine blood pressure was markedly reduced from 189 +/- 6/117 +/- 3 (mean +/- SE) to 151 +/- 5/91 +/- 3 mm Hg (P less than .001). New T-wave inversions developed in 6 of 23 (26%) subjects, but blinded evaluation of 2-D echocardiograms revealed no new wall motion abnormalities. Wall motion score, which at pretreatment was abnormal in 11 of 23 patients, improved significantly after nifedipine from 1.4 +/- 0.1 to 1.2 +/- 0.1 (P less than .05). Therefore, rapid and marked reduction of blood pressure with nifedipine is accompanied by a high incidence of asymptomatic T-wave inversions which are not accompanied by left ventricular wall motion abnormalities, suggesting that significant myocardial ischemia did not occur.
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PMID:Isolated T-wave abnormalities and evaluation of left ventricular wall motion after nifedipine for severe hypertension. 206 77

We investigated the clinical and pathophysiologic characteristics in patients with vasospastic angina who developed syncope and/or experienced aborted sudden death (SD). Vasospastic angina was diagnosed using the methylergonovine test. Syncope was found in 32 (10.4%) patients among 309 who were admitted to our institute in a one-year period. The most frequent cause of syncope was ventricular tachycardia which was found in 10 (31.2%) of the 32 patients. The next important cause of syncope was vasospastic angina which was found in 7 patients (21.8%). Among the 7 patients with vasospastic angina who experienced one or more syncopal episodes, there were 3 patients with aborted SD, 3 with syncope and one with shock. Cardiovascular collapse was observed in 4. Interior wall ischemia was found in 5 and anterior wall ischemia in 2 during the methylergonovine test. None of the 7 patients had significant coronary stenosis. Two patients had no prodromal symptom such as chest pain. Our results suggest that coronary artery spasm may be one of the most frequent cardiovascular diseases that causes syncope which is not always accompanied by a prodromal symptom. Therefore, coronary spasm should be distinguished in patients with unexplained syncope or aborted SD.
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PMID:Clinical characteristics and possible role of coronary artery spasm in syncope and/or aborted sudden death. 207 44

We performed exercise thallium-201 myocardial scintigraphy in 32 patients with angina pectoris to study the incidence of perfusion defects, who had no significant organic stenosis on coronary angiography. None of them had myocardial infarction or cardiomyopathy. Thallium-201 myocardial scintigraphy and 12-lead ECG recording were performed during supine bicycle ergometer exercise. Perfusion defects in thallium-201 scintigrams in SPECT images were assessed during visual analysis by two observers. In the coronary angiograms obtained during intravenous infusion of nitroglycerin, the luminal diameter of 75% stenosis or less in the AHA classification was regarded as an insignificant organic stenosis. Myocardial perfusion defects in the thallium-201 scintigrams were detected in eight (25%) of the 32 patients. Six of these eight patients had variant angina documented during spontaneous attacks with ST elevations in standard 12-lead ECGs. Perfusion defects were demonstrated at the inferior or inferoposterior regions in six patients, one of whom had concomitant anteroseptal defect. The defects were not always accompanied by chest pain. All but one patient demonstrating inferior or inferoposterior defects showed ST depression in leads II, III and aVF on their ECGs, corresponding to inferior wall ischemia. The exception was a case with right bundle branch block. Thus, 25% of the patients with angina pectoris, who had no evidence of significant organic stenosis on their coronary angiograms, exhibited exercise-induced perfusion defects in their thallium-201 scintigrams. Coronary spasms might have caused myocardial ischemia in these patients.
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PMID:[Exercise-induced thallium-201 myocardial perfusion defects in angina pectoris without significant coronary artery stenosis]. 209 48

From a pool of patients, treated because of cardiac diseases on ward for 4 years, 8 subjects, the mean age of which amounted to 46 (SD 12) years, showing stable angina pectoris in usual physical activity, were chosen. In these patients widespread examinations including invasive procedures had not been evident for one of the well defined heart diseases. In two patients dysrhythmias appeared during standardized exercise test while in four other subjects acute cardiac findings consisted of chest pain, significant depression of ST segments or inversion of T waves were observed. One patient had a normal result of the exercise test. A myocardial thallium-201 imaging was performed in four subjects. In three patients imaging showed questionable or mild signs of ischemia. The result suggest the existence of unknown shapes in coronary heart disease, the origin of which is possibly connected with a disorder of microvascular smooth muscle reactivity.
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PMID:[The possible significance of coronary vascular resistance in chronic ischemic heart disease]. 209 86

Three cases of cardiotoxicity manifested by chest pain, tachycardia, respiratory distress, and electrocardiographic changes simulating acute myocardial infarction or ischemia were observed during the course of combination chemotherapy with etoposide, cisplatin, and continuous infusion of 5-fluorouracil in patients with advanced non-small cell lung cancer. There was no cardiac enzyme elevation. A similar but rare clinical syndrome has been described in association with 5-fluorouracil infusion as a single agent or in combination with other chemotherapeutic agents. We describe the cases and review their possible pathogeneses and clinical implications.
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PMID:Electrocardiographic changes simulating acute myocardial infarction or ischemia associated with combination chemotherapy with etoposide, cisplatin, and 5-fluorouracil. 209 95

To elucidate the prevalence and features of painless myocardial ischemia among diabetic patients, 44 consecutive patients with angiographically-documented coronary artery disease and positive treadmill tests were examined. They were 26 with diabetes and 18 without it. Painless myocardial ischemia was defined as the absence of chest pain with 1 mm or more ST segment depression during the exercise stress tests. The severity of ischemia was determined by the magnitude of the ST segment depression. Painless myocardial ischemia was observed in 18 of the 26 (69%) diabetics, and in three of the 18 (17%) non-diabetics (p less than 0.005). The frequency of painless ischemia in the diabetics was relatively high regardless of the severity of ischemia, while painless ischemia was less frequent in the non-diabetics with severe ischemia. With a level of 2.5 mm ST depression, 11 of 12 (92%) diabetics were free of pain compared to four of 11 (36%) non-diabetics (p less than 0.01). Absence of chest pain during the exercise tests was not concordant with prior angina in diabetics, as opposed to non-diabetics in whom both clinical and exercise-induced angina developed concordantly. The diabetic patients without chest pain had a higher prevalence of three major diabetic complications such as neuropathy, nephropathy and retinopathy compared to those developing chest pain (p less than 0.025). It was concluded that in diabetics, painless myocardial ischemia is frequently observed during exercise stress tests and its prevalence is relatively high regardless of the severity of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Painless myocardial ischemia in diabetic patients with coronary artery disease: evaluations by treadmill exercise tests]. 210 4

Patients with angina-like chest pain without evidence of epicardial coronary artery disease or coronary arterial vasospasm are becoming increasingly recognized. These are often related to noncardiac causes including esophageal, musculoskeletal, and hyperventilatory or panic states. However, recently a subgroup of such patients are being recognized as having true myocardial ischemia and chest pain on the basis of diminished coronary microvascular vasodilatory reserve (microvascular ischemia or Syndrome X). The authors describe such a patient who was found to have replication of anginal pain associated with a reversible ischemic defect on thallium 201 imaging during atrial pacing, suggesting ischemia in this myocardial segment. Resolution of angina and ST segment electrocardiographic changes of ischemia occurred with cessation of pacing. We believe this is the first report of a patient with this form of myocardial ischemia diagnosed by this method and should be considered in patients with anginal chest pain after significant coronary artery disease and coronary vasospasm have been excluded.
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PMID:Syndrome of diminished vasodilator reserve of the coronary microcirculation (microvascular angina or syndrome X): diagnosis by combined atrial pacing and thallium 201 imaging--a case report. 211 63

Myocardial ischemia usually presents with chest pain, the characteristics of which are well known. However, anginal pain may be absent during true ischemia, an entity known as painless or silent myocardial ischemia. Does this type of ischemia have special clinical, angiographic or ergometric characteristics after posterior myocardial infarction (MI)? In order to answer this question 183 consecutive patients with recent posterior MI who had undergone coronary angiography and who had positive exercise stress tests on bicycle ergometers were separated into two groups depending on whether they had experienced at least one episode of pain after the acute phase of myocardial infarction or during the exercise stress test (Group S: 83 patients, average age 54 +/- 10 years) or not (Group A: 100 patients, average 54 +/- 8 years). The following parameters were commoner in Group A: cigarette smoking, heart rate and load developed during exercise stress testing provoking electrical signs of ischemia, single vessel disease on coronary angiography, long-term medical treatment. On the other hand, the following parameters were statistically more frequent in Group S: hypercholesterolemia, preinfarction angina, degree of ST depression during exercise testing, reperfusion of the distal vessels of the occluded artery responsible for the infarct by a collateral circulation, triple vessel disease and surgical treatment. However long-term follow-up (average 3 years) shows that mortality and recurrence of MI are similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Painless myocardial ischemia. Comparison of 2 groups of patients with a positive exercise test after myocardial infarction]. 212 30


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