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

The relationship between long-term propranolol hydrochloride therapy and subsequent coronary bypass operation was prospectively investigated in 119 patients who were grouped three ways: propranolol therapy continued in full dosage to operation (group A), propranolol therapy discontinued or tapered 24 to 72 hours preoperatively (group B), and no preoperative propranolol therapy (control group). During preoperative hospitalization, one patient in each group A and the control group suffered an increase in anginal symptoms compared with 15 patients in group B, three of whom also had new ventricular arrhythmias. During anesthesia up to the period of cardiopulmonary bypass, 26% of group A patients showed signs of ischemia (eg, ST segment deviation or ventricular arrhythmias) as compared with 51% of the control group and 70% of group B. Hypotension and bradycardia were not more common in group A patients. No differences among groups were noted in case of emergence from bypass, need for cardiac stimulants, or mortality.
JAMA 1978 Sep 29
PMID:Preoperative propranolol therapy and aortocoronary bypass operation. 30 9

Surgical teaching has suggested that renal nonfunction of more than a few days' duration usually precludes success of revascularization procedures. The efficacy of delayed renal revascularization in selected cases has been reported. In this case, the intravenous pyelogram, renal scan, and ureteral catheterization verified nonfunction 30 days before surgical correction of essentially complete atheromatous occlusion of the renal artery. Postoperative studies conducted six weeks and 18 months postoperatively showed normal bilateral renal function. Current temporal limitations on attempts to preserve renal tissue may be too stringent. Revascularization of kidneys may be successful after prolonged periods of ischemia.
JAMA 1977 Dec 05
PMID:Successful renal revascularization after prolonged nonfunction. 57 88

Creatine kinase (CK), lactic dehydrogenase (LDH), and more recently their isoenzyme determinations (CK-MB and LDH1) have been useful adjuncts in verification of myocardial injury. To determine whether DC cardioversion affects these serum enzyme levels, we recorded total CK, total LDH, CK-MB, and LDH1 levels serially during 24 hours following elective DC cardioversion in 18 patients without cardiac ischemia. New postcardioversion elevations in total CK and total LDH levels were small and occasional: CK (one of 18 patients), LDH (four of 18 patients). Elevations of CK-MB or LDH1 following cardioversion did not develop in any of the patients. Therefore, new CK-MB or LDH1 elevations associated with arrhythmias must result from myocardial damage to DC cardioversion.
JAMA 1978 Jan 09
PMID:Direct current cardioversion. Effect on creatine kinase, lactic dehydrogenase and myocardial isoenzymes. 57 71

Ten cases of lower-extremity emboli originated from proximal, ulcerated atherosclerotic plaques. Two distinct clinical presentations were seen. Embolization of cholesterol-rich debris was usually widespread and lodged in terminal arteries, producing either focal digital ischemia or livedo reticularis of the extremity. By contrast, thrombi arising from mural erosions were larger and produced a picture indistinguishable from emboli of cardiac origin. Biplanar aortography was essential in making the correct diagnosis. Anticoagulation has not prevented recurrent embolization. Endarterectomy or graft replacement of the diseased arterial segment is the preferred method of treatment. Lumbar sympathectomy is a useful adjunct when persistent cutaneous ischemia is present.
JAMA 1979 Feb 23
PMID:Lower-extremity arterial emboli from ulcerating atherosclerotic plaques. 76 46

Most out-of-hospital cardiac arrests result from the sudden onset of a sustained ventricular arrhythmia in the absence of a new myocardial infarction. Individuals who survive cardiac arrest are at high risk for recurrent arrhythmias and sudden unexpected death. To prevent recurrent cardiac arrest, effective treatment must be provided during hospitalization after the initial episode. Caring for the survivor of cardiac arrest requires a detailed clinical investigation to define the underlying cardiac anatomy and left ventricular function and to elucidate the mechanism and characteristics of the patient's arrhythmia. Appropriate antiarrhythmic therapy, such as drugs or a nonpharmacological intervention (eg, implantable cardioverter-defibrillator), is then selected based on these considerations. In addition, ischemia is treated aggressively with beta-adrenergic blocking agents and, when appropriate, with surgical coronary artery revascularization.
JAMA 1991 Feb 13
PMID:Current treatment of patients surviving out-of-hospital cardiac arrest. 189 76

Extended ambulatory electrocardiographic monitoring in the patient's customary environment provides clear evidence of circadian patterns in myocardial ischemic episodes. In patients with effort angina, the highest activity occurs between 6 AM and noon. This coincides with peaks in diurnal variation of frequency of acute myocardial infarction, stroke, and sudden death. A number of potential underlying common triggering mechanisms, including catecholamine secretion, sympathetic nervous system activity, blood pressure, heart rate, cortisol secretion, and aggregability of platelets, exhibit similar surges. As a result of these coinciding morning peaks, myocardial oxygen demand is increased and oxygen supply reduced after a person arises in the morning. Attention to this vulnerable period is merited in the timing and choice of medication, both to prevent or reduce ischemia and to modify potential disease-triggering mechanisms.
JAMA 1991 Jan 16
PMID:Circadian variations in myocardial ischemia. Implications for management. 198 40

Pharmacologic stress imaging has increasingly been employed as an alternative to exercise imaging for detection of coronary artery disease and risk stratification particularly in patients who are unable to perform adequate exercise. Sensitivity and specificity of thallium 201 scintigraphy using intravenous dipyridamole infusion as a stress for coronary artery disease detection average 85% and 91%, respectively. Dipyridamole imaging is also useful for differentiating between ischemia and scar and identifying patients who have an increased risk for subsequent cardiac events. Dipyridamole imaging is particularly useful for preoperative risk stratification in patients undergoing surgery for peripheral vascular or aortic disease. Dipyridamole imaging is also useful for identifying residual myocardial ischemia after myocardial infarction and detecting restenosis after coronary angioplasty. Adverse side effects of dipyridamole are promptly reversed by aminophylline. Dipyridamole stress can also be employed in association with echocardiography for detection of ischemia-induced regional wall motion abnormalities.
JAMA 1991 Feb 06
PMID:Pharmacologic stress imaging. 198 15

The symptoms of organic disease vary widely among patients with the same tissue abnormality, because the experience of a symptom is shaped by the patient's perceptual and cognitive style. Thus, the relationship between myocardial ischemia and chest pain is variable in that many patients experience pain without ischemia and many others exhibit ischemia without pain-termed "silent" or "asymptomatic ischemia." Although the nature of the ischemic event may be important in determining the degree of associated pain, we suggest more study of the individual who perceives the event. Myocardial ischemia may not generate a spontaneous report of chest pain because the patient is generally hyposensitive to visceral sensation; because he or she is coping with the threat of heart disease by denying the evidence of it--ie, denying the pain to deny the disease; or because the patient misunderstands the cause and significance of a vague or ambiguous cardiac sensation, normalizing the symptom and misattributing it to a nonpathologic cause.
JAMA 1990 Sep 05
PMID:Silent myocardial ischemia. Is the person or the event silent? 198 46

The area of cerebral resuscitation has become an exciting area of research in critical care medicine. It is a complicated field, however, which has seen attempts to protect the brain using a single therapy such as barbiturates ultimately disappoint investigators in the field. It is likely that much more work needs to be done in understanding the intracellular metabolic and biochemical effects of ischemia before therapies can be designed that are likely to be effective. This work might ultimately require knowledge of how ischemia or hypoxia interrupt cellular RNA and DNA machinery before these effective therapies can be developed. Before we are discouraged by the difficulty of the task, however, it is useful to review how much progress has been made in understanding the pathophysiology of ischemic brain injury in the past decade, so that we may be challenged to continue our efforts in this exciting area of critical care medicine.
JAMA 1989 Jun 02
PMID:Current concepts in brain resuscitation. 256 85

Reperfusion following lower-torso ischemia in humans leads to respiratory failure manifest by pulmonary hypertension, hypoxemia, and noncardiogenic pulmonary edema. The mechanism of injury has been studied in the sheep lung lymph preparation, where it has been demonstrated that the reperfusion resulting in pulmonary edema is due to an increase in microvascular permeability of the lung to protein. This respiratory failure caused by reperfusion appears to be an inflammatory reaction associated with intravascular release of the chemoattractants leukotriene B4 and thromboxane. Histological studies of the lung in experimental animals revealed significant accumulation of neutrophils but not platelets in alveolar capillaries. We conclude that thromboxane generated and released from the ischemic tissue is responsible for the transient pulmonary hypertension. Second, it is likely that the chemoattractants are responsible for leukosequestration, and, third, neutrophils, oxygen-derived free radicals, and thromboxane moderate the altered lung permeability.
JAMA 1989 Feb 17
PMID:Reperfusion pulmonary edema. 221 74


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