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)

Clinical experience with the Percor percutaneous intraaortic balloon (IAB) was reviewed in 722 cases performed by 59 clinicians (35 surgeons and 24 cardiologists). Compared with standard IABs, Percor was judged to provide easier insertion by 88% of clinicians, easier femoral-iliac passage by 29%, easier aortic passage by 36%, and easier final positioning by 19%; the Percor IAB was rated more difficult in these respects by 2-5% of users; the rest of the responders found no significant difference in these measures. Technical problems included an inability to negotiate sclerotic vessels in 12.6%, delayed hemostasis in 1.9%, and the need for surgical repair of the arteriotomy site in 2%. Medical complications included peripheral ischemia in 5.3%, emboli in 3.6%, arterial dissection in 1.9%, dislodged arterial plaque in 1.1%, perforation of the arterial tree in 1.0%, local femoral thrombosis in 1.0%, and poor intraoperative hemostasis in 0.3%. Local wound infection, ischemic amputation or neuropathic sequelae were not reported. Mechanical counterpulsation with Pecor was equivalent to that of standard IABs, but by subjective judgments, 80% rated Percor more desirable and 47% safer; 3% rated it less desirable and 10% less safe. With Percor, earlier clinical use of IAB pumping was seen by 73%, and new or additional indications were recommended by 19%.
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PMID:Clinical evaluation of the Percor percutaneous intraaortic balloon: cooperative study of 722 cases. 708 45

Seventy-three patients with an angiographically identified asymptomatic stenosis (greater than 50%) and/or ulceration of the common carotid bifurcation have been followed from 6 months to 10 years (average 4 years). All patients had previously undergone contralateral carotid endarterectomy for a transient ischemic attack (TIA) or minor stroke in that carotid territory. During follow-up, 22 patients (30%) developed new symptoms of cerebral ischemia. Twelve developed ischemia referable to the previously asymptomatic side (10 TIA's, 2 strokes). Six developed recurrent ischemic symptoms in the territory of the previously symptomatic and operated carotid artery (2 TIA's, 4 strokes). Five developed ischemia in the vertebro-basilar territory (2 TIA's, 3 strokes). Thirteen patients (17%) died during follow-up, including 6 from cardiovascular disease and 3 from stroke. In our series the incidence of stroke in the territory of a significant asymptomatic carotid plaque was low (3%). Patients were as likely to develop stroke in the territory of a previously operated carotid artery (5%) with asymptomatic carotid lesions is to keep them under review and to consider endarterectomy only if appropriate ischemic symptoms (which are most likely to be TIA's) develop.
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PMID:The natural history of asymptomatic carotid bifurcation plaques. 710 45

Angina pectoris and asymptomatic myocardial ischemia are part of the spectrum of coronary heart disease. Not the presence or absence of angina determines the future of the patient, but repeated ischemia and the progression of the coronaropathy. This progression is neither linear with time, nor is the moment of plaque rupture foreseeable. Silent myocardial infarctions increase with age and are very frequent in diabetics. In patients without neuropathy but with asymptomatic myocardial ischemia the central pain threshold is higher than in patients with angina pectoris. The best noninvasive test for the detection, localization and estimation of extension of myocardial ischemia, be it pain-free or symptomatic, is 201-thallium scintigraphy, combined with the exercise ECG. The fight against all amendable cardiovascular risk factors and pharmacotherapy are the first steps, if asymptomatic myocardial ischemia is suspected. Augmented dyspnea on effort and rhythm disturbances are indicators of advanced multivessel heart disease. Under these circumstances coronary angiography is indicated, and further treatment should follow the generally accepted rules such as for patients with angina pectoris.
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PMID:[Asymptomatic ischemia--an important part of the spectrum of coronary disease]. 748 31

Compared with pathologic studies coronary angiography is a relatively insensitive technique to detect early atherosclerosis. Coronary angioscopy is a new technique providing direct information on luminal vessel surface. To determine whether coronary angioscopy may detect the presence of atherosclerotic disease on angiographically normal coronary segments, 52 patients underwent a study with coronary angioscopy before coronary angioplasty. The mean age was 59 +/- 10 years; 46 patients were men and 6 were women. The reason for coronary angioplasty was unstable angina in 36 patients, stable angina in 8 patients, and silent ischemia in 8 patients. In seven patients angiography revealed luminal irregularities on the coronary segment proximal to the culprit lesion, and all these patients also had proximal disease as demonstrated by coronary angioscopy. In the remaining 45 (87%) patients angiography revealed a smooth-vessel contour proximal to the target lesion. On quantitative angiography these "normal" coronary segments measured 2.8 +/- 0.4 mm in luminal diameter. In 30 (67%) of these patients angioscopy revealed proximal disease on the vessel wall, but in 15 (33%) patients the luminal surface of these segments also appeared normal on angioscopy. Disease as detected by angioscopy in angiographically normal segments included yellow plaque in 19 patients, mural thrombus in 5, mixed plaques in 4, and small flaps in 2 patients. In eight patients coronary angioscopy detected that atherosclerotic disease extended proximally from the target lesion, but in the remaining 22 patients the angioscopic findings appeared to be discrete and well separated from the angiographic lesion. All these plaques were relatively small and did not protrude into the coronary lumen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Findings of coronary angioscopy in angiographically normal coronary segments of patients with coronary artery disease. 748 60

Atheromatous plaque material containing cholesterol crystals may dislodge and cause distal ischemia. To characterize atheroembolic renal failure, we retrospectively evaluated all patients at the Massachusetts General Hospital from 1981 to 1990 with both renal failure and histologically proven atheroembolism after angiography or cardiovascular surgery. Over the 10-year period, 52 patients were identified. They tended to be elderly men with a history of hypertension (81%), coronary artery disease (73%), peripheral vascular disease (69%), and current smoking (50%). Within 30 days of their procedure, only 50% of patients had cutaneous signs of atheroembolism, and 14% had documented blood eosinophilia. Urinalysis was often abnormal. Hemodynamically unstable patients died shortly after their procedure, yet renal function in the remainder continued to decline over 3 to 8 weeks. Patients who received dialysis had a higher baseline serum creatinine than those who did not (168 +/- 44 mumol/L versus 133 +/- 18 mumol/L, p = 0.02), with dialysis starting a median of 29 days after the procedure. Patients with renal failure due to atheroembolism alone, as opposed to multiple renal insults, were more likely to recover renal function (24% versus 3%, p = 0.03) and had a lower risk of death during the 6 months after their procedure (log-rank p = 0.002). Renal failure due to procedure-induced AE is characterized by a decline in renal function over 3 to 8 weeks. This time course is not consistent with most other iatrogenic causes of renal failure, such as radiocontrast or nephrotoxic medications, which present earlier and often resolve within 2 to 3 weeks after appropriate intervention.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atheroembolic renal failure after invasive procedures. Natural history based on 52 histologically proven cases. 750 Aug 98

Ischemic electrocardiographic changes were recorded within 2 hours of admission using a 12-lead electrocardiographic continuous monitor with a 20-second scanning interval and an alarm mode for asymptomatic events. Blood samples were obtained at admission and at the moment of asymptomatic events (group A). In the other patients who did not develop ischemia, a second blood sample was taken 12 hours later (group B). We determined prothrombin time, activated partial thromboplastin time, clotting factor VIII activity, tissue plasminogen activator activity, tissue plasminogen activator inhibitor-1, cross-linked fibrin degradation product, and thrombin-antithrombin III complexes. There was a statistically significant difference between group A and B patients when the basal samples were analyzed for thrombin-antithrombin III (p = 0.046) and d-Dimer (p = 0.005). Prothrombin fragment 1 + 2 were significantly reduced, and d-Dimer was elevated when basal blood samples were compared with the second sample in patients who developed silent events (p = 0.008 and 0.055, respectively). A plasma concentration of thrombin-antithrombin III complex was also significantly decreased when sample 2 was compared with the basal blood sample (p = 0.039). Five recurrent episodes of angina and 2 nonfatal infarctions occurred, and 4 urgent revascularization procedures were performed in group A. In group B, there was only 1 nonfatal infarction (p = 0.01). The results of the present study suggest that a time-dependent thrombotic process is detectable in the blood stream as a cyclic movement. Further studies are needed to determine if some other factors, such as intensive shear stress in the vessel wall, may activate plaque instability during asymptomatic episodes.
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PMID:Time significance of acute thrombotic reactant markers in patients with and without silent myocardial ischemia and overt unstable angina pectoris. 761 Nov 44

Directional coronary atherectomy (DCA) is the sole technique for the in vivo study of coronary artery plaques which are responsible for myocardial ischemia. The technique confers the following advantages to the pathologic study of plaque samples: the brevity, in general, of the interval between acute myocardial ischemia and sampling of the guilty plaque; the absence in samples of autolytic phenomena (such as those that affect autopsy samples), an effect that enables the use of conventional histopathology, immunohistochemistry and molecular biology; the certainty with which the researcher can identify, and thus sample, the truly guilty lesions. The drawbacks of the technique are: the fragmentation of the plaque; the difficulty the pathologist has in correctly orientating the samples in the embedding phase, in distinguishing pre- from post-procedural lesions, and in providing a detailed description of the findings. Given the foregoing, the diagnostic information to which DCA sampling enables access is as follows: plaque derivation--the recognition of whether tissue removed with DCA originates from eccentric or concentric, atheromatous of fibrosclerotic, calcified or not calcified plaques; histopathology of coronary lesions that cause ischemia with regard to: evidence of acute events, such as thrombosis, ulceration and hemorrhage, thrombus composition, when it occurs, and definition of its age and presence of material deriving from the vascular wall that lies beyond the plaque; identification and immunophenotypical characterization of inflammatory infiltrates. As regards research, the main implications of DCA are for the study of the pathogenetic mechanisms that lead to plaque instability in acute ischemic syndromes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diagnostic and research potential of directional atherectomy]. 763 16

Direct evidence from pathologic-anatomical studies in victims of sudden cardiac death has been given for acute ischemia (caused by either an acute thrombus, plaque fissuring or an organizing thrombus) to play a major role in the genesis of sudden cardiac death. Furthermore, indirect data on the effects of drugs in the setting of acute myocardial infarction have demonstrated that treating patients with beta-blocking agents is more beneficial than treating them with a pure anti-arrhythmic drug such as lidocaine. Whereas lidocaine, which also reduces the incidence of ventricular fibrillation in the setting of acute myocardial infarction, may produce an excess of mortality, beta-blockers reduce ventricular fibrillation and are associated with a prolonged survival. Further, indirect evidence on the role of ischemia in ventricular arrhythmias is given in patients with chronic ischemic heart disease by several studies on coronary revascularization and by studies on antiarrhythmic drugs versus beta-blockers in the same situation. In conclusion, there is clear evidence from studies of coronary revascularization and from studies on drug intervention in different patient populations with ischemic heart disease at risk for ventricular arrhythmias and/or for sudden cardiac death that ischemia plays an important role in the genesis of these arrhythmias.
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PMID:Therapeutic consequences of newer studies addressing the problem of myocardial ischemia and ventricular arrhythmias. 763 2

The effects of acute ischemia on conduction velocities in the longitudinal (theta L) and transverse (theta T) fiber axis were determined from epicardial activation patterns, recorded with 48 bipolar electrodes (plaque electrode, 25 x 35 mm) on the left anterior ventricular wall of eight dogs and the posterior wall of seven dogs. During left ventricular stimulation (cycle length = 300 msec) in the center of the plaque electrode, theta L, theta T, and the ratio of longitudinal to transverse conduction velocities (theta L/T) were measured before and 2 to 5 minutes after occlusion of the left anterior descending coronary artery or the left circumflex coronary artery. During the control state theta L was greater than theta T demonstrating anisotropic properties of cardiac muscle, not only in the anterior but also in the posterior wall. During acute ischemia theta L and theta T were decreased from the control value and theta T was decreased by a greater extent than theta L resulting in an increase in theta L/T from 1.83 +/- 0.31 (mean +/- SD) to 2.19 +/- 0.36 in the anterior wall and from 1.58 +/- 0.17 to 1.92 +/- 0.28 in the posterior wall. During ventricular fibrillation some lines of conduction block were parallel to the long axis of epicardial muscle fiber bundle and the others were perpendicular. In conclusion, acute ischemia increased anisotropic conduction (theta L/T) in the epicardial ventricular muscle mainly due to greater reduction in theta T, in the anterior and the posterior wall. This augmented anisotropic ventricular conduction may have some relation to the initiation of ventricular fibrillation during acute ischemia.
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PMID:Effects of acute ischemia on anisotropic conduction in canine ventricular muscle. 769 Sep 34

Myocardial ischemia tends to be self-propagating, and minor events such as plaque rupture can lead to the catastrophic sequelae of myocardial infarction and death. The biology of the endothelium and the cardiac myocyte is crucial to the development of these vicious circles. The abnormal responses of the endothelial cell in atherosclerosis tend to provoke and propagate ischemia, and because of the limited metabolic reserve of the myocyte, even short periods of ischemia can lead to left ventricular dysfunction and arrhythmias. This article examines the clinical implications of the disordered biology of the endothelial cell and the myocyte that is the basis for ischemic left ventricular dysfunction.
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PMID:The vicious circle of ischemic left ventricular dysfunction. 772 18


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