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

The quality of the morphological analysis of myocardial and coronary alterations depends essentially on the method chosen for the heart dissection. Even if previous postmortem coronary angioplasty is not feasible, the best results are obtained by transverse sectioning of the ventricles in a bread-loaf fashion subsequent to formalin-fixation and serial cross-sectioning of the coronary arteries, with decalcification in addition if necessary. The distribution pattern of disseminated myocardial necrosis, the longitudinal, circumferential and transmural extent of infarction, its age and sequelae and its correlation to the coronary supplying areas can be evaluated with better accuracy than by dissecting the heart chambers according to the flow of blood. Cross-sectioning of coronary arteries with preservation of their luminal shape allows proper examination of the degree and extent of luminal narrowing, plaque hemorrhage, parietal and occluding thrombi and the effects and complications of angioplastic procedures or bypass surgery. Transverse sectioning of the heart is a prerequisite for adequate examination following sudden cardiac death and short-term territorial ischemia. Full-thickness samples of the ventricular walls, taken systematically with respect to coronary narrowing and coronary supplying areas, enable identification of early myocardial damage.
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PMID:[Macroscopic and microscopic heart preparation in ischemic heart diseases]. 779 68

To assess the prognostic contribution of exercise two-dimensional echocardiography in patients undergoing elective coronary angioplasty, 60 patients (44 males, 16 females, mean age 61 years) were enrolled in this study. The series included 31 patients with single-vessel disease, 23 with two vessel, and 5 with three vessel disease. After successful PTCA, they underwent stress echocardiographic testing either by treadmill (n = 23) or bicycle ergometry (n = 37), performed with digital continuous loop technique. A wall motion index (WMI) was calculated at rest and at peak stress. According to WMI values, the study population was divided into three groups: patients with normal WMI both at rest and stress (Group 1); patients with abnormal baseline WMI without change at stress (Group 2) and abnormal WMI diagnostic of stress-induced ischemia (Group 3). During the follow-up period, minimum of 1 year, 21 patients complaining of recurrent angina or chest discomfort, had repeat angiography: in 13 of these, typical restenosis of a previously dilated artery was found; 2 patients had progression of atherosclerotic plaque and in 6 the angiogram showed a good result of PTCA. Thirteen patients with restenosis or progressive disease underwent repeat PTCA. In this group, only 2 belonged to Group 1, 4 to Group 2, and 7 to Group 3. Thus, a linear correlation between the WMI value post-angioplasty and the clinical course could be documented (p = 0.001). Stress echocardiography was superior to stress ECG in both negative predictive value (88 and 77% respectively) and positive predictive value (73 versus 50%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Risk stratification for restenosis after coronary angioplasty by means of exercise echocardiography. 785 32

The case report describes an acute total ischemia of both legs in a young otherwise healthy woman. Based on the patient's history, the physical findings and further investigations, the differential diagnosis is discussed. The emergency procedure with a successful desobliteration of a strictly localized arteriosclerotic plaque by Fogarty catheter was followed by open thrombendarterectomy 10 days later because of a persistent stenosis. Finally the clinical manifestations of such rare occlusive disease of the aorta are discussed as well as the bilateral ischemic syndrome of the lower extremities originally described by Leriche in 1940.
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PMID:[Acute Leriche syndrome in a previously healthy woman: differential diagnosis of embolic occlusion]. 787 6

In western countries, acute myocardial infarction is the commonest cause of morbidity and mortality [19]. An occlusive coronary thrombus on an ulcerated atherosclerotic plaque in the coronary arteries is the etiological event in more than 90% of patients with Q-wave myocardial infarction [38]. The underlying abnormality in non-Q-wave myocardial infarction is often a ruptured atherosclerotic plaque, which acts as a nidus for the deposition and activation of platelets. In this case, thrombosis occurs, but may not be totally occlusive, or an early spontaneous recanalization may occur. On the other hand, some clinical trials showed that a prolonged treatment with antiplatelet drugs significantly reduces the recurrence of coronary ischemia. Thus, atherosclerosis is a necessary condition for myocardial infarction, but it is not sufficient in that it usually needs the occurrence of thrombosis. However, only 25-30% of these thrombotic events are prevented by the administration of antiplatelets drugs. In recent years, epidemiological studies identified some hemostatic parameters whose abnormalities may help predict the risk of ischemic events: fibrinogen [14], plasminogen activator inhibitor-1 (PAI-1) [3], lipoprotein(a) [46], anticardiolipin antibodies (ACA) and lupus anticoagulant (LA) [10], leukocyte count [34], blood viscosity [34]. Some of these, such as fibronogen and PAI-1 are acute-phase proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma predictors of ischemic complications of atherosclerosis: open issues. 806 Dec 44

Peripheral obstructive arterial disease (POAD) of the lower limbs is the third main complication of atherosclerosis, after coronary artery disease and cerebrovascular disease. In 15-20% of cases POAD have an unfavourable evolution toward critical leg ischemia (CLI). This clinical condition is characterized by the onset of rest pain and/or trophic cutaneous lesions until gangrene appears. In some cases amputation is needed. The pathophysiological, clinical and therapeutic aspects of CLI were recently discussed in two Consensus Conferences held in Berlin in 1989 and in Rudesheim in 1991, with the elaboration of a final draft published on circulation. CLI appears when peripheral perfusion critically decreases due to macro and microcirculatory alterations. Atherosclerotic plaque is the primum movens, but often there are more plaques in sequence along the ilio-femoro-popliteal axis. The pathophysiological and clinical consequences are more severe if the stenosis is haemodynamically important, after a rapid progression of plaque growth or when thrombotic complications develop. The reduction in distal perfusion induces troubles in the microcirculation and an embalancement between the microvascular defense system (MDS) and the microvascular flow regulating system (MFRS) with endothelial dysfunction, platelet and leucocytes activation, worsening of blood viscosity due to the increase in fibrinogen levels and to the red cells deformability changes, activation of coagulation and impairment of fibrinolysis. So, a vicious circle appears with further worsening of distal perfusion and onset of trophic lesions. A further worsening of CLI can derive from local recurrent infections particularly frequent in diabetic patients.
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PMID:[The physiopathology of critical ischemia of the lower limbs]. 811 25

Patients surviving acute myocardial infarction are susceptible to heart failure, recurrence of angina, reinfarction, arrhythmias, and sudden cardiac death. Most deaths occur in the first six months after infarction. Advancing age is the most important nonmodifiable prognostic factor for long-term prognosis, whereas left ventricular function assessed clinically or measured as either ejection fraction or end-systolic volume is the most important modifiable factor. Other significant long-term prognostic factors include: postinfarction angina at rest, inducible ischemia during exercise testing with or without radioisotope imaging, severity and extent of coronary artery disease, patency of the infarct-related artery, late ventricular arrhythmias, decreased heart rate variability, cigarette smoking, hypercholesterolemia, and diabetes mellitus. Identification of these adverse prognostic factors permits risk stratification and enables physicians to determine the most appropriate and cost-effective treatment. Most patients should have a stress test for inducible ischemia and a non-invasive (echo or radionuclide) assessment of left ventricular function. For high-risk patients such as those with prior infarction, heart failure, early postinfarction angina, or frequent late ventricular arrhythmias, coronary angiography and ventriculography prior to discharge are recommended. Assessment of late potentials and heart rate variability will help identify a subgroup of patients at risk for ventricular arrhythmias and cardiac death. However, a more accurate prediction of reinfarction is not possible at present, and no reliable test for atherosclerotic plaque instability has been developed.
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PMID:Factors affecting outcome after recovery from myocardial infarction. 819 87

Cerebrovascular disease remains an important cause of disability and death in the geriatric population. This paper reviews the current state of knowledge with respect to the pathogenesis and medical and surgical treatment of carotid atherosclerosis. The majority of strokes are probably due to embolization from an ulcerated atherosclerotic plaque at the carotid bifurcation rather than from ischemia produced by global reduction in cerebral blood flow related to obstruction of the carotid arteries. Ultrasonography is an appropriate screening examination, but most vascular surgeons consider contrast angiography to be essential in the preoperative evaluation. Large clinical trials have evaluated the efficacy of stroke prevention by carotid endarterectomy in symptomatic patients. The North American Symptomatic Carotid Endarterectomy Trial clearly demonstrated a benefit of surgery in stroke prevention as compared with optimal medical therapy after only 18 months of follow-up. The European Carotid Surgery Trial and a VA Cooperative Study produced similar conclusions. Much less information is available concerning the patient with carotid atherosclerosis who has no cerebral symptoms. No convincing evidence that surgery is beneficial has yet been demonstrated, but a large multicenter clinical trial (Asymptomatic Carotid Atherosclerosis Study) remains in progress.
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PMID:Surgical management of carotid artery atherosclerotic disease. 821 52

A 41-year-old man suffered 3 episodes of transitory left leg ischemia before he was admitted with right brachial artery embolism. The diagnostic evaluation (i/v DSA, CT Scan) revealed a mass in the ascending aorta which was removed under hypothermic cardiocirculatory arrest. Histologically the mass was shown to be a thrombus adjacent to a arteriosclerotic plaque.
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PMID:[Thrombosis of the ascending aorta--a rare cause for recurrent arterial embolism]. 822 47

Proper understanding of the pathologic process of a ruptured plaque followed by thrombus formation, with acute assessment of the deranged pathophysiology of the coronary circulation as a sequel, remains the basis for rational therapy of cardiac ischemia. With the advent of better thrombolytic regimens, improved direct reperfusion via angioplasty, and streamlined recognition/admission procedures, therapeutic strategies for dealing with acute myocardial infarction have once more turned to the options for early therapy. From recent studies of out-of-hospital thrombolysis or immediate percutaneous transluminal coronary angioplasty, the position is reinforced that "early" means the first 100 minutes. It is hoped that the large Global Utilization of Streptokinase and t-PA for Occluded Arteries (GUSTO) study, which specifically analyses the effect of early reperfusion by optimal alteplase and actilyse (recombinant tissue-type plasminogen activator [rt-PA]) versus streptokinase regimens will confirm this essential concept once and for all. Thus, when appropriate therapy--depending in the local availability of facilities--is promptly given, further reductions in myocardial infarction size and ventricular dysfunction can be achieved, resulting in mortality rates < 5%, at substantial savings in ever more expensive healthcare resources. "Early is < 100 minutes; later may be too late or too costly."
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PMID:Expanding indications for thrombolytic therapy in acute myocardial infarction. How late is too late, and how early is early: the clinician's view of the first 100 minutes. 827 56

Disruption of an atherosclerotic plaque in coronary arteries with a minor stenosis is the usual stimulus for acute coronary thrombosis and myocardial infarction. In this article the pathogenesis of arterial thrombosis and contributions of local arterial wall substrates, the rheology of blood flow, systemic factors, and the critical role of thrombin in the formation of thrombus are discussed. More potent antithrombotic therapy may accelerate exogenous thrombolysis, allows endogenous thrombolysis, and should reduce recurrent infarction and ischemia and death, as well as need for coronary revascularization. Maximal antithrombotic therapy for acute myocardial infarction includes an intravenous bolus of heparin at 100 U/kg followed by an intravenous infusion--at 1,200 U/hr for patients weighing 60-80 kg, 1,300 U/hr for those weighing > 80 kg, and 1,000 U/hr for those weighing < 60 kg (or 17 U/kg/hr)--to maintain the activated partial thromboplastin time at 2-3 times control (60-90 sec) for at least 5-7 days. To convert intravenous to subcutaneous administration, use 14,000-17,000 U every 12 hours and initially overlap the intravenous infusion by 2 hours. The loading dose of aspirin on admission to the hospital is 160 mg followed by 80 mg/day. High-risk patients should be considered for conversion of heparin to warfarin therapy for at least 3 months at an international normalized ratio of 2.5-4.0 for the prevention of recurrent ischemia, reinfarction, death, thromboembolism, reactivation of thrombosis, and reduced necessity for revascularization.
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PMID:Conjunctive antithrombotic therapy for thrombolysis in myocardial infarction. 827 64


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