Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The long-term course of angina and the electrocardiographic signs of ischemia were assessed in 13 patients (10 women and 3 men, mean age 49 +/- 6 years) with typical angina pectoris, positive exercise tests, no evidence of coronary spasm and angiographically normal coronary arteries (syndrome X). Clinical and electrocardiographic parameters as well as results of exercise testing and 24-hour electrocardiographic monitoring were assessed at presentation and after a mean follow-up of 6.3 years (range 3 to 9). Mean number of anginal episodes and nitroglycerin consumption per week were similar at presentation and at the last follow-up. Furthermore, no significant difference was noted in heart rate-systolic blood pressure product at 0.1 mV of ST-segment depression (20,363 +/- 5,747 vs 21,649 +/- 5,687 beats/min x mm Hg), at angina (19,223 +/- 5,680 vs 20,126 +/- 6,023 beats/min x mm Hg) and at peak exercise (22,057 +/- 5,669 vs 22,868 +/- 6,122 beats/min x mm Hg). Time to 0.1 mV of ST-segment depression, to angina and to peak exercise was also similar (595 +/- 163 vs 631 +/- 184 s, 524 +/- 156 vs 571 +/- 168 s and 671 +/- 168 vs 718 +/- 186 s, respectively). The number of episodes of ST-segment depression greater than or equal to 0.1 mV during electrocardiographic monitoring was similar at presentation and follow-up (31 vs 25) as was the proportion of painful episodes (39 vs 36%). None of the patients developed major coronary events or cardiomyopathy during follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Long-term variability of angina pectoris and electrocardiographic signs of ischemia in syndrome X. 274 23

The efficacy of the adenosine receptor blocker aminophylline on exercise capacity in patients with effort ischemia and documented coronary artery disease has been previously documented. In this study the effect of aminophylline on effort electrocardiographic (ECG) alterations and chest pain was tested in eight patients with syndrome X (anginal chest pain on effort, ischemic ECG changes during exercise, positive dipyridamole test, normal epicardial coronary arteries on angiography and absence of coronary spasm after ergonovine). After double-blind, randomized intravenous infusion of aminophylline (6 mg/kg body weight over 15 min) or placebo (20 ml of saline solution over 15 min), the eight patients with syndrome X underwent an upright bicycle exercise stress test on 2 consecutive days. After aminophylline, there was an increase in effort tolerance (aminophylline 7.7 +/- 1.2 min of exercise versus placebo 5.6 +/- 0.9, p less than 0.01) paralleled by an increase of the rate-pressure product (mm Hg x beats/min x 1/100) at 0.1 mV of ST segment depression or at peak exercise (aminophylline 278 +/- 55 versus placebo 230 +/- 24, p less than 0.05). Aminophylline provoked the abolition of ECG signs of ischemia in all eight patients. Thus, at a dosage that should effectively inhibit adenosine receptors, aminophylline infusion exerts a beneficial effect on exercise-induced chest pain and ischemia-like ECG changes in syndrome X. This effect occurs possibly through the prevention of myocardial flow maldistribution elicited by inappropriate adenosine release during effort in the presence of increased coronary resistance at the level of small intramural coronary arteries. This study, however, does not document the ischemic nature of effort-induced pain and ECG alterations in syndrome X.
 ...
PMID:Improved exercise capacity with acute aminophylline administration in patients with syndrome X. 280 3

A recent report showed that during Holter monitoring of patients with syndrome X (typical anginal pain, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries), 50% of episodes of ischemic ST-segment depression were painful. This proportion is considerably higher than that in patients with chronic stable angina, which is about 30%. A significantly lower threshold and tolerance to painful stimuli was seen in a group of patients with chronic stable angina in whom 50% of episodes were painful compared with a group in whom only 5% of episodes were silent. Hence, patients with syndrome X may have enhanced sensitivity to painful stimuli. To investigate whether this difference was due to a lower threshold for painful stimuli in general, 12 patients with syndrome X and 10 (age- and sex-matched) with chronic stable angina were studied using the same battery of painful stimuli. Patients with syndrome X had a significantly lower threshold and tolerance for forearm ischemia (-36%, p less than 0.05, and -40%, p less than 0.001) and electrical skin stimulation (-37%, p less than 0.01, and -35%, p less than 0.001); the cold pressor test did not show significant differences (-7%, p = 0.391, and -1%, p = 0.818). Thus, patients with syndrome X in this study had significantly lower threshold and tolerance values for forearm ischemia and for electrical skin stimulation. These differences in sensitivity to pain may partly explain a higher incidence of painful ischemic episodes detected by ambulatory electrocardiographic monitoring during unrestricted daily life.
 ...
PMID:Pain threshold and tolerance in women with syndrome X and women with stable angina pectoris. 363 Sep 32

Nineteen patients with syndrome X (typical exertional angina, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) underwent continuous 48-hour electrocardiographic (ECG) monitoring during unrestricted daily life. Fifty-eight ischemic episodes of at least 0.1 mV of ST-segment depression were observed in the same ECG leads that showed ST depression during stress testing: 28 (48%) were accompanied by anginal pain and 30 (52%) were asymptomatic. No significant differences were found between painful and silent ST-segment depression with regard to the number of episodes, their temporal distribution, magnitude, duration or heart rate (HR) at onset of ST-segment depression. In the minute preceding ischemic ST shifts, HR did not change in 33% of episodes or increased by less than 10 beats/min in 28%. HR at onset of ST depression was significantly lower during ambulatory ECG monitoring than during exercise testing (98 +/- 18 vs 117 +/- 18 beats/min, p less than 0.01). During ambulatory monitoring, 85 episodes of sinus tachycardia (exceeding by 10 to 80 beats/min the HR that triggered ischemia during exercise testing) occurred in the absence of angina or ST-segment shifts. The results of this study suggest that in patients with syndrome X, myocardial ischemia frequently develops during daily life; silent ischemia is an important component of this syndrome; and increased oxygen demand in the presence of impaired coronary vasodilatory capacity is not the only cause of myocardial ischemia. Active mechanisms that transiently reduce coronary flow may act and explain occurrence of angina at rest and with minimal exertion.
 ...
PMID:Transient myocardial ischemia during daily life in patients with syndrome X. 378 14

Studies in patients with microvascular angina (MA) or the cardiologic syndrome X have shown a hyperinsulinemic response to an oral glucose challenge, suggesting insulin resistance and a role for increased serum insulin in coronary microvascular dysfunction. The aim of the present study was to examine whether patients with MA are insulin-resistant. Nine patients with MA and seven control subjects were studied. All were sedentary and glucose-tolerant. Coronary arteriography was normal in all participants, and exercise-induced coronary ischemia was demonstrated in all MA patients. A euglycemic, hyperinsulinemic clamp was performed in combination with indirect calorimetry. Biopsy of vastus lateralis muscle was taken in the basal state and after 4 hours of euglycemia and hyperinsulinemia (2 mU.kg-1.min-1). The fasting level of "true" serum insulin was significantly higher (43 +/- 6 v 22 +/- 3 pmol/L, P < .02) and the rate of insulin-stimulated glucose disposal to peripheral tissues was lower in patients with MA (13.4 +/- 1.0 v 18.2 +/- 1.4 mg.kg fat-free mass [FFM]-1.min-1, P < .02) due to a decrease in nonoxidative glucose metabolism (8.4 +/- 0.9 v 12.5 +/- 1.3 mg.kg FFM-1.min-1, P < .02). No difference was found in glucose or lipid oxidation rates between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Insulin-resistant glucose metabolism in patients with microvascular angina--syndrome X. 761 46

A 53-year-old female presented with disabling chest pain. The pain had most of the characteristics of ischemic pain; however, the results of the initial clinical investigation were consistent with the diagnosis of syndrome X. That is, her treadmill exercise test was positive but her coronary angiogram was normal. A dipyridamole-thallium test resulted in severe chest pain, marked ST abnormalities, but no evidence of any focal reduction in flow. A dipyridamole stress echocardiogram revealed that left ventricular function was entirely normal during the dipyridamole-induced pain and ST segment abnormalities, making ischemia an unlikely cause for either. To attempt to account for this paradox, the hypothesis was generated that both the pain and ST segment abnormalities were due to a primary abnormality of adenosine metabolism rather than secondary to ischemia. Accordingly, adenosine-MIBI scans were done with and without pretreatment with aminophylline. Infusion of adenosine virtually immediately resulted in crushing chest pain and profound ST abnormalities again without any evidence of focal abnormalities of MIBI estimated flow. By contrast, administration of adenosine after pretreatment with aminophylline failed to produce either chest pain or ST abnormalities. Moreover, long term therapy with aminophylline almost entirely relieved the symptoms which had been so distressing. This case indicates that there is a subset of patients with syndrome X--in which faults in adenosine metabolism result in excessive adenosine accumulation or effect and this results, in turn, in adenosine-induced ischemic-like chest pain and adenosine-induced ST abnormalities. There is, however, no actual ischemia of the myocardium. Given the known effects of adenosine on coronary flow, the problem in this subset of patients appears to be equivalent to an attack of myocardial migraine and blockers of adenosine action might be of help to other patients with a similar pathophysiology for their chest pain.
 ...
PMID:Report of a patient with syndrome X due to excessive adenosine effect: myocardial migraine without myocardial ischemia. 772 47

To evaluate whether the ischemic threshold has a circadian rhythm in patients with syndrome X, we analyzed 90 episodes of ST depression detected on 24-hour Holter recordings of 12 such patients. Ischemic threshold was considered as heart rate (HR) at 1 mm ST depression. To correct for differences in basal HR among patients, however, the ischemic threshold was also calculated as a normalized index of HR at 1 mm ST depression: [(HR at 1 mm ST-24-hour modal HR)/24-hour modal HR]-100. Mean hourly values of both absolute and normalized HRs at 1 mm ST depression were obtained by grouping and averaging respective values of all episodes detected in every hour of the day in all patients. Chronobiologic analysis was performed by single cosinor method. A significant circadian rhythm was found for HR (mesor 76 beats/min, amplitude 10 beats/min, acrophase at 2:16 P.M., p < 0.001), number of episodes of ST depression (mesor 3.75, amplitude 2.9, acrophase at 2:45 P.M., p < 0.001) and cumulative time of ischemia, with a high correlation of distributions. Episodes of ST depression showed a double peak initially in the morning, and again in the afternoon. Both raw and normalized values of HR at 1 mm ST depression also had a significant circadian variation in ischemic threshold, which was lower in the night and early morning hours, progressively increased until the first afternoon hours, and subsequently decreased in the evening.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Circadian variation of ischemic threshold in syndrome X. 790 Jun 60

This study describes the results of Dobutamine stress echocardiography in 10 patients with Syndrome X. The diagnosis of Syndrome X was made on the basis of the presence of exertional angina, positive exercise stress test, negative ergonovine stress test and normal coronary arteries at angiography. All patients underwent Dobutamine stress echocardiography after interruption of any antianginal therapy. Dobutamine was infused starting with a dose of 5 mcg/kg/min over 3 minutes with incremental steps of 5 mcg/kg/min every 3 minutes up to a maximal dose of 40 mcg/kg/min. Two-dimensional echocardiography and 12-lead electrocardiography was monitored during the infusion of the drug. Nine patients received the maximal dose while one patient prematurely stopped the test for the occurrence of side effects. None of the ten patients developed segmental left ventricular wall motion abnormalities indicative of myocardial ischemia; ST-segment depression diagnostic for ischemia developed in 30% of patients; angina was elicited in one of these patients and in two additional patients. A hyperkinetic response to Dobutamine infusion involving all the segments of the left ventricle was observed both in patients with and without chest pain or electrocardiographic changes. In patients with Syndrome X Dobutamine induces a hyperkinetic left ventricular response indicative of normal contractile reserve despite the presence in some cases of angina and electrocardiographic signs of ischemia.
 ...
PMID:Results of dobutamine stress echocardiography in patients with syndrome X. 796 53

Abnormal constriction of coronary resistive vessels can induce angina and myocardial ischemia. The possibility that a microvascular vasomotor dysfunction could cause ischemia is in contrast with the well-known traditional notion that a metabolically induced vasodilation could compensate for the effect of an epicardial coronary stenosis. Vasoconstrictor stimuli can plausibly act on vessels situated immediately proximal (prearterioles) to those that can be dilated by ischemia metabolites (arterioles). This functional 2-compartment model of resistive vessels is based on the ability of different substances to cause opposite actions on resistive vessels with different sizes. The possible mechanisms of prearteriolar dysfunction, observed in patients with syndrome X, single vessel disease after a successful PTCA and in a subset of chronic stable patients include: an organic reduction of total vascular section; vascular smooth muscle hyperreactivity to heterogeneous constrictor stimuli; an impaired flow-mediated endothelium-dependent vasodilation (possibly due to a reduced NO and/or EDHF synthesis). The first and third hypothesis can only account for anginal episodes at effort while the second model could explain episodes occurring at rest and without an increase in heart rate. Those mechanisms causing an imbalance between myocardial oxygen supply and demand, induce an increased release of adenosine in order to promote a compensating vasodilation. Adenosine can possibly avoid the occurrence of ischemia but, being a powerful algogenic stimulus, causes pain. It is worth noting that the presence of patchy prearteriolar dysfunction induces areas with excessive release of adenosine. Since total vascular section is extremely large a massive adenosine spill-over can occur with a consequential boosting of algogenic and vasodilatory effect.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Mechanisms of coronary microvascular dysfunction]. 802 13

Several studies have shown evidence of the key role of the endothelium in modulating the tone of epicardial coronary vessels, in the different manifestations of coronary artery disease. Recently, the role of endothelium-dependent vasodilation has been focused, because clinical observations have suggested that myocardial ischemia might be caused or aggravated by inappropriate vasoconstriction of resistance vessels. An abnormal endothelium-dependent vasodilation, either of epicardial and of coronary microvasculature, has been documented in patients with syndrome X and in patients with history of hypertension and left ventricular hypertrophy. Vasoconstriction of the small coronary vessels is probably the mechanism underlying the impaired increase of coronary blood flow during atrial pacing and the wide variations of the ischemic threshold in some patients with chronic stable angina. In patients with variant angina, the endothelial function seems abnormal only in the conductance vessels. It is likely that the endothelial dysfunction of the small coronary arteries be present in many clinical situations in which a discrepancy between a mild atherosclerosis of epicardial coronary artery and signs of ischemia exists, as it has been observed early after successful angioplasty and after coronary artery reperfusion during acute myocardial infarction.
 ...
PMID:[Endothelial dysfunction in ischemic syndromes]. 802 14


<< Previous 1 2 3 4 5 6 7 Next >>