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

The aim of this prospective study was to assess the prognostic and most suitable management of AMI in elderly patients (age > or = 75 years). From September 1988 to August 1991, 129 such patients (pts) were evaluated: 35 (27%) were admitted to CCU because of arrhythmias or severe hemodynamic complications; 94 (73%) were addressed, according to bed availability, to CCU (55 pts) or Cardiology Ward (39 pts), where all patients underwent continuous ECG monitoring for at least 72 hours. Age, gender, history of previous angina or myocardial infarction, presence of chest pain or ECG ischemia on admission, site and extent of AMI, delay on admission, CPK-MB peak, recurrent angina, arrhythmias, heart failure, emotional disorders, hospital mortality and length of hospital stay were compared. Our results show that elderly patients who suffered from complicated AMI were at high risk for death and severe in-hospital complications. No significant prognostic differences were observed between the two groups with uncomplicated AMI. Thus hospitalization in the Cardiology Ward seems to be valuable, safe and well tolerated in our population of elderly patients with AMI, and without initial complications.
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PMID:[Management and prognosis of acute myocardial infarct in advanced age: comparison of the cardiac intensive care unit and the cardiology ward]. 129 24

Six patients (2 males and 4 females, mean age of 46 years) with X syndrome were reported in this paper. All patients presented with typical exertional angina pectoris. In 4 patients the angina had a variable threshold of onset, it often occurred at rest and occasionally nocturnally. The electrocardiogram during chest pain showed ST segment depression of more than 0.05-0.1 mV in all 6 patients. The treadmill or bicycle ergometer exercise test was positive in 4 cases (ST segment depression > 0.1 mV), equivocal in 1 (ST segment < 0.1 mV) in whom the 201Tl exercise myocardial perfusion scan showed sign of ischemia, and negative in 1 in whom atrial pacing at heart rate of 135 beats/min induced angina and ST segment depression of 0.1-0.15 mV. Echocardiograms and X ray chest films revealed no sign of ventricular hypertrophy or enlargement. The 201Tl exercise myocardial perfusion scan was performed in 5 patients, which showed signs of ischemia in 4 patients and suspected to have ischemia in 1. Left ventriculograms and coronary angiograms were normal in all 6 patients. Ergonovine provoking test (total dose of 0.4 mg) was negative in 5 patients, it was not performed in 1 in whom there was no evidence of coronary artery spasm by angiogram during appearance of electrocardiographic ischemic changes and chest pain. Left ventricular endomyocardial biopsy was performed in 1 patient, which showed significant smooth muscle cell proliferation in the medial layer of a small artery with diameter of 62.5 mu which produced narrowing of the lumen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[X syndrome--report of six cases]. 130 21

To elucidate the pathological aspects of silent myocardial ischemia, we studied 24 patients with ischemic heart disease who had culprit lesions in the left anterior descending artery (LAD). We determined the presence of myocardial ischemia and measured coronary wedge pressures (CWP; mmHg) and collateral circulation and ST deviation on the ECG (intracoronary ECG: ic-ECG, and surface ECG; mm) after balloon inflation during PTCA intervention. The study subjects included 9 with exertional angina, 10 with post-infarction angina, and 5 with Cohn type II angina. During 78 balloon inflations, the group of ischemic symptoms (Group S) occurred in 40% of all cases, the group without ischemic symptoms (Group A) constituted 45%, and the Cohn type II specific for ischemic symptoms accounted for 15%. The relationship between CWP (X-axis) and ST deviation (Y-axis) of ic-ECG was: Y = -0.46X + 20.19 (r = -0.59; p < 0.01), and the relationship between CWP and ST deviation of the surface ECG was: Y = -0.12X + 6.58 (r = -0.42; p < 0.01). Thus, a negative correlation was confirmed between them. Furthermore, similar results were obtained for Groups S and A. Based on this relationship, the pain threshold was estimated. In Group S, CWP exceeded 34 mmHg, i.e., ischemia was expected to be mild because of good collateral circulation, but an average ST deviation accompanying ischemic symptoms was observed. However, in Group A, CWP was less than 24 mmHg, i.e., ischemia was expected to be severe due to poor collateral circulation, but an average ST deviation lacking ischemic symptoms was observed. Comparison of these results showed that the pain threshold observed from the ST deviation of ic-ECG was 6.0-6.5 mm and that of the surface ECG was 2.6-2.8 mm. From these threshold values, the ST deviations during 12 balloon inflations in the Cohn type II were evaluated. Because 100% of ic-ECG and 75% of surface ECG exhibited values exceeding the threshold values, it was concluded that the cause of the Cohn type II was an increase of the pain threshold. ST deviations of the ic-ECG for Group S and the Cohn type II were 12.0 +/- 6.7 and 9.8 +/- 2.7 mm, respectively, and ST deviations of the surface ECG were 4.7 +/- 2.4 and 3.5 +/- 1.7 mm, respectively. Since there were no significant differences between Group S and the Cohn type II, it was concluded that the ischemic degree of the Cohn type II was approximately the same as that of Group S.
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PMID:[Trial assessment of pain threshold]. 130 72

Bicycle ergometer exercise was used to induce ischemia in 20 patients with stable angina pectoris (SAP). Superoxide dismutase (SOD) blood concentrations, free radical generation (by the SOD-inhibitable reaction of ferricytochrome C), malondialdehyde (MDA) plasma concentrations, the unfractionated leucocyte filterability rate and the filterability rates of the granulocyte and mononuclear sub-fractions (using a positive pressure filtration system and 5 mu diameter Nuclepore filters), were monitored before and after exercise in the patients and in 18 matched controls. At the onset of ischemia a significant increase in the level of MDA plasma concentrations and significant decreases in both SOD blood concentrations and the SOD-inhibitable reduction of ferricytochrome C indicated oxygen free radicals had been released in the SAP patients. These changes were associated with significant impairments of granulocyte and unfractionated leucocyte filterabilities and with morphological evidence of granulocyte activation.
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PMID:Leucocytes and free radicals in stable angina pectoris. 131 70

The reports of 8 patients with acute or subacute abdominal pain related to venous mesenteric ischemia were reviewed. None of the patients presented local or regional predisposing factors for venous thrombosis. In 4 patients, a localized segment of ischemic small bowel (median length 125 cm; range: 30-350) was resected without immediate anastomosis and postoperative anticoagulation therapy was given. Two of these patients developed recurrent ischemia involving the bowel adjacent to the stoma, treated successfully in 1 case by a repeat resection. The 4 other patients hospitalized with intestinal obstructive symptoms (1 case) or abdominal angina (3 cases) were treated by long term anticoagulation in 3 cases and artificial nutrition in 2 cases. None of them developed mesenteric infarction with a median follow up of 34 months. In 7 of the 8 patients, a coagulopathy was found: primary myeloproliferative disorder (1 case), hypercoagulation state (5 cases), autoimmune hemolytic anemia (1 case). These observations suggest that venous mesenteric ischemia included two different entities on the basis of clinical and morphological criteria: mesenteric infarction and subacute transient ischemia without bowel infarction. Most of apparently idiopathic cases of acute or subacute venous mesenteric ischemia are related to hypercoagulation states requiring a long term anticoagulation.
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PMID:[Syndromes of venous mesenteric ischemia: infarction and transient ischemia]. 133 Jul 93

The Nifedipine Gastro-Intestinal Therapeutic System (GITS) Circadian Anti-ischemia Program (N-CAP) was designed to test the effect of nifedipine GITS as monotherapy or in combination with a beta-adrenergic blocking agent on the circadian pattern of angina and silent ischemia in patients with chronic stable angina. At 118 sites in the United States, 1,174 patients were screened for entry into this study. To be eligible for participation patients were required to have at least two episodes of angina a week and at least two episodes of myocardial ischemia during 48-h ambulatory electrocardiographic (ECG) monitoring during the baseline placebo period. A total of 207 patients completed all phases of the study. Beta-blockers were continued in those patients already receiving them. In this 7- to 10-week single-blind placebo withdrawal study, a 1-week placebo run-in was followed by up to 5 weeks of single-blind titration with nifedipine GITS, a 4-week efficacy phase with an established dose and a final single-blind 2-week placebo withdrawal period. Ambulatory ECG monitoring was performed at the end of each placebo phase and at the end of the efficacy phase with a digital monitoring device that was validated in a pilot study. Overall, nifedipine GITS significantly reduced the weekly number of anginal episodes from 5.7 to 1.8 (p = 0.0001) and the number of ischemic events from 7.3 to 4 (p = 0.0001) reported during the 48-h monitoring periods, with a significant increase in both during the placebo withdrawal period. The baseline circadian pattern of ischemia showed an early morning peak and a secondary peak in the afternoon. Nifedipine GITS significantly reduced ischemia during the 48-h period when administered as monotherapy or in combination with a beta-blocker. Patients were also randomized to receive nifedipine GITS in either a morning or an evening dose. The two regimens resulted in equal anti-ischemic benefit. The primary side effect of nifedipine GITS was edema, which was dose related. In summary, nifedipine GITS reduced the number of anginal and ischemic episodes when given alone or in combination with a beta-blocker. Nifedipine GITS had a sustained effect: a single daily dose was effective over 24 h regardless of whether it was administered in the morning or evening. This study also suggests that combination therapy with nifedipine GITS and a beta-blocker is especially efficacious in reducing ischemia.
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PMID:Attenuation of the circadian patterns of myocardial ischemia with nifedipine GITS in patients with chronic stable angina. N-CAP Study Group. 135 May 96

Recent investigations of SMI occurring during daily life have advanced our understanding of the pathophysiology of myocardial ischemia. These contributions have directed our attention away from "chest pain" alone and physical exertion as the central provoking factor toward transient myocardial ischemia and its broader triggers and consequences. Transient myocardial ischemic episodes, the majority of which are silent, are found in a subset of patients with any clinical manifestations of CAD (eg, stable angina, unstable angina, myocardial infarction, and sudden death), as well as in those patients with CAD who are and have been totally asymptomatic. These episodes are an independent predictor of increased risk for future cardiac events. Most medical therapy and revascularization therapies have the potential to prevent or relieve these silent episodes; however, we do not yet know which method is superior in reducing SMI episodes or preventing future cardiac events. Furthermore, the benefit of reducing SMI versus the cost and potential morbidity of these chosen therapies is not known. At least three trials are now underway to examine some of these concerns (Table 2). Focus on pain relief alone does not appear to be an adequate approach to alter outcome in patients with CAD and may prove insufficient to control SMI. Until these issues are resolved, we believe a conservative approach to the management of patients with CAD is warranted. Documentation of ischemia (painful or painless) is essential. Three general principles should be kept in mind. First, the presence of detectable ischemia is of central importance. This information should be used in the overall risk assessment of the patient. Second, the level of concern or aggressiveness of treatment should be based on the risk associated with the ischemic abnormalities documented (Table 3). The exercise stress test is the most useful to begin this process. The detection of ischemic-type ST-segment depression, either silent or painful, at a low workload (eg, less than or equal to 120 beats per minute or less than or equal to 6.5 metabolic equivalents [METS]) implies high risk for adverse outcome. Likewise, these ST-segment changes occurring in leads that reflect multiple coronary artery distribution, of greater than 2 mm in magnitude and persisting for greater than 6 minutes, are all markers for high risk. Thallium redistribution defects occurring at low work loads, in multiple areas, associated with increased lung uptake and enlargement of the cardiac pool all imply high risk.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Treatment strategies for daily life silent myocardial ischemia: a correlation with potential pathogenic mechanisms. 135 7

Treatment of silent ischemia is still controversial, because of the lack of studies showing improvement of prognosis with therapy. However, silent ischemia is an independent predictor of poor prognosis. Therefore significant ischemia has to be investigated to determine the therapeutic strategies as for patients with angina pectoris. The medical therapy has been reported successful with nitrates, beta-blockers and calcium canal blockers. The same applies for surgical therapy and PTCA. The target has to be to reduce myocardial ischemia and to ameliorate the prognosis.
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PMID:[Therapy of silent ischemia]. 135 5

In order to investigate the mechanism and treatment of angina decubitus, 20 patients (18 men and 2 women aged 36-70 years) were studied during hospitalization. All patients were found to have an increased heart rate x systolic blood pressure product before the onset of angina decubitus, indicating that this type of angina pectoris belongs to the category of effort angina. Of the 11 patients investigated by continuous hemodynamic monitoring, 3 had significant progressive increases in pulmonary artery systolic pressure (PASP) and pulmonary artery diastolic pressure (PADP) before onset: their episodes of angina could not be completely controlled by digoxin and diuretics, but quickly subsided after beta blockers were added. Among the other 8 patients, PADP increased slightly in 5 and remained unchanged in 3 cases before onset: these patients had no manifestations of LV dysfunction, and beta blockers combined with coronary vasodilators produced satisfactory effects. These results indicate that LV failure is not a major factor in the pathogenesis of angina decubitus. The LV diastolic dysfunction seen in 8/11 cases may have been related to LV hypertrophy caused by long-term hypertension or chronic persistent ischemia.
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PMID:Hemodynamic observation and treatment approach for patients with angina decubitus. 136 74

Cardioprotection is a broad term; this short review deals with six aspects: 1. Secondary prevention of myocardial infarction (MI) has been shown for beta-blockers in both early and late intervention studies. Dihydropyridine calcium antagonists are associated with an excess incidence of coronary events, whereas non-dihydropyridines prevent reinfarction provided left ventricular (LV) function is adequate; dihydropyridines tend to increase heart rate and stimulate the sympathetic and renin-angiotensin systems. 2. Primary prevention of MI has been shown for beta-blockers in younger/middle-aged hypertensives but not in the elderly. Diuretics, by contrast, possibly increase the risk of coronary events in younger/middle-aged hypertensives but significantly reduce coronary events in older hypertensives. These results might be explained by the larger, noncompliant left ventricle of the elderly hypertensive, which, in the absence of overt ischemia, responds poorly to beta-blockade (further enlargement with increased wall stress and impaired coronary reserve), while diuretics have the opposite effect. Primary prevention of coronary events in patients with chronic angina is likely to occur with beta-blockers, while studies with calcium antagonists have shown a significant excess of coronary events. 3. Ischemic events occurring during the "vulnerable" period between 7 and 10 AM (when sympathetic activity is maximal) are significantly reduced by beta-blockers but not by calcium antagonists. 4. Stress-induced myocardial necrosis in humans is markedly reduced by beta-blockers. 5. Coronary risk factors, such as elevated blood lipids, hyperglycemia, and insulin resistance, are possibly adversely affected by diuretics and beta-blockers, with the former also increasing heart rate, plasma renin activity, and plasma catecholamine levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antihypertensive drugs and cardioprotection. 136 81


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