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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A prognostic index for acute myocardial infarction was developed from noninvasively accessible parameters, gathered prospectively within 24 h from the onset of symptoms in 185 consecutive patients. Of the 35 patients who died in hospital, 30 had power failure. The items subjected to discriminant function analysis were: sex, age, number of previous infarctions, present infarction transor nontransmural, heart rate, systolic arterial pressure (SAP), left ventricular ejection time (LVET), cardiothoracic ratio, and grade of pulmonary venous congestion scored 0-3 (PVC0-3). The items possessing the best predictive power were, in the order of their strength: age, SAP, LVET and PVCO-3; i.e., hemodynamically, afterload, stroke volume and preload. The discriminant function (DF) giving the prognostic score was: DF=3.9Xage(yr)-1.3X SAP (mm Hg) - 1.4 X LVET (msec) + 25.3 X PVC0-3 + 775.3 Score 550 was exceeded by 87% of the patients dying of power failure and only 16% of the survivors, and it was less in 84% of the survivors and 13% of those dying. To test the validity of the index it was applied to another series consisting of 100 consecutive patients and very similar results were obtained, suggesting that the index is of practical value in predicting hemodynamic deterioration early and by simple noninvasive means.
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PMID:Assessment of immediate prognosis in acute myocardial infarction by a new noninvasive hemodynamic index. 127 7

The goal of this study was to assess the effect of gallopamil on left ventricular (LV) diastolic function early after acute myocardial infarction (AMI). Gallopamil was compared with placebo and atenolol in two different groups of patients. Study patients, 2 days after experiencing their first AMI, in Killip class I and stable sinus rhythm, were randomized in a crossover, double-blind sequence to receive (a) gallopamil (50 micrograms/kg over 5 min) or placebo (i.v. 10-ml bolus, with a time interval of 90 min); and (b) gallopamil (50 micrograms/kg over 5 min) or atenolol (5 mg over 5 min), with a time interval of 24 h. Group I and group II consisted of 28 patients (26 men and 2 women; mean age 55 +/- 9 years) and of 14 patients (13 men and 1 woman; mean age 56 +/- 10 years), respectively. All the patients were treated with thrombolysis within 6 h from the onset of symptoms. Doppler echocardiographic examinations were performed as follows: at baseline (B) and 15 min after administration of gallopamil bolus and placebo bolus, in group I; at baseline before gallopamil (BG) and atenolol (BA), and 15 min after each bolus in group II. The following echo-Doppler parameters were calculated, at each examination: the early and late transmitral peak velocity ratio (E/A), the early and late velocity integral ratio (Ei/Ai), the peak filling rate normalized to mitral stroke volume (nMPFR), and the LV isovolumic relaxation time (IVRT), which was normalized to an 800-ms R-R cycle length in the patients in group II. Mean blood pressure (MBP) and heart rate (HR) were also measured.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diastolic ventricular dysfunction in noncomplicated acute myocardial infarction: the influence of gallopamil. 128 57

Neuropeptides are the most abundant chemical messengers in the brain and their major role seems to be the modulation of amine and amino acid neurotransmission. This appears to be achieved at many sites by the co-release of peptide with the primary transmitter. The presynaptic biochemistry and physiology of neuropeptides ensure that neuromodulation is highly plastic with almost infinite adaptive potential. The recent development of novel drugs (termed peptoids) that mimic or block neuropeptide function have opened up new clinical approaches to a number of conditions. Thus high efficacy kappa opioid-receptor agonists such as CI-977 (enadoline) have potential for the treatment of pain and stroke whilst the development of highly selective and bioavailable cholecystokinin B (CCK-B) antagonists such as CI-988 ([R-(R*,R*)]-4-[[2-[[3-(1H-indol-3-yl)-2-methyl-1-ox6-2- [[tricyclo[3.3.1.1.3.1]dec-2-yloxy)carbonyl]amino]propyl]ami no]-1-phenethyl]amino-4-oxobutanoic acid) have offered new insights into the mechanisms underlying and the treatment of anxiety disorders and drug abuse. In general it appears that peptoids may offer a greater selectivity of drug action when compared to amino acid/amine based compounds. Peptoid antagonists appear to be relatively free of side effects possibly because neuropeptide systems are only activated under very selective conditions. Peptoid agonists on the other hand can exert extremely powerful actions on brain function and this may be related to the key position neuropeptide receptors occupy in the hierarchy of chemical communication in the brain.
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PMID:Neuropeptides. Function and clinical applications. 131 55

Antiphospholipid antibodies have been suggested as markers for a high risk of recurrent cardiovascular events in young survivors of an acute myocardial infarction. However, there are few data to confirm or refute this hypothesis. In a cohort study, we have measured anticephalin (aCEPHA) and anticardiolipin (aCL) antibodies in a group of patients surviving an acute infarct. Of 597 patients studied, 13.2% were IgG or IgM aCEPHA positive compared with 4.4% of a reference population (n = 158; p = 0.002). In a multivariate analysis, adjusted for major cardiovascular risk factors, neither aCEPHA (IgG or IgM) nor a CL (IgG or IgM) was an independent risk factor for mortality, reinfarction, or non-haemorrhagic stroke. Although an increased proportion of survivors of a myocardial infarction have antiphospholipid antibodies, the presence of such antibodies is not a risk factor for subsequent coronary or cerebrovascular thrombosis.
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PMID:Antiphospholipid antibodies after myocardial infarction and their relation to mortality, reinfarction, and non-haemorrhagic stroke. 135 86

41,299 patients entering 914 hospitals up to 24 h (median 4 h) after the onset of suspected acute myocardial infarction were randomised between streptokinase (SK: 1.5 MU infused over about 1 h), tissue plasminogen activator (tPA, duteplase: 0.60 MU/kg infused over about 4 h), or anisoylated plasminogen-streptokinase activator complex (APSAC), anistreplase: 30 U over about 3 min). All patients were to receive aspirin (162 mg/day enteric-coated), with the first tablet chewed for rapid and full antiplatelet effect. Half of all patients were randomly allocated subcutaneous calcium heparin (12,500 IU starting at 4 h and given twice daily for 7 days or until prior discharge) in addition to aspirin, and the other half were to receive aspirin alone. ASPIRIN PLUS HEPARIN VERSUS ASPIRIN ALONE--The addition of heparin to aspirin was associated with an excess of transfused or other major non-cerebral bleeds (1.0% aspirin plus heparin vs 0.8% aspirin alone; 2p < 0.01) and of definite or probable cerebral haemorrhage (0.56% vs 0.40%; 2p < 0.05), but with no significnat differences in total stroke (1.28% vs 1.18%). Reinfarctions were slightly less common among those allocated aspirin plus heparin (3.16% vs 3.47%; 2p = 0.09). There was no signficant difference in the pre-specified endpoint of 35-day mortality (2132 [10.3%] aspirin plus heparin vs 2189 [10.6%] aspirin alone). During the scheduled heparin treatment period there were slightly fewer deaths in the aspirin plus heparin group (days 0-7 in hospital: 1534 [7.4%] vs 1633 [7.9%]; 2 p = 0.06), with a slight convergence by day 35 (598 further deaths [3.1% of survivors] vs 556 [2.9%]). The pattern was similar to that observed in the GISSI-2 trial, so that in both trials combined there was a significant reduction in mortality during the scheduled treatment period (2071 [6.8%] vs 2239 [7.3%]; 2p < 0.01). This indicates avoidance of 5 deaths (SD 2) per 1000 patients allocated this high-dose subcutaneous heparin regimen in addition to aspirin, but some of any early benefit may be lost after heparin ceases, with no significant mortality advantage in days 0-35 (both trials: 3100 [10.0%] vs 3172 [10.2%]) or during follow-up to 6 months. SK VERSUS APSAC--APSAC was associated with significantly more reports of allergy causing persistent symptoms and of non-cerebral bleeds, but not of transfused bleeds or of reinfarctions. There was a slight excess of strokes with APSAC (1.04% SK vs 1.26% APSAC; 2p = 0.08), much of it appearing soon after treatment started (strokes during days 0-1: 0.50% SK vs 0.73% APSAC; 2p < 0.02) and being attributed to cerebral haemorrhage (0.24% SK vs 0.55% APSAC; 2p < 0.0001). No significant difference was observed in reinfarction (3.47% SK vs 3.55% APSAC). There was no significant mortality difference during days 0-35, either among all randomised patients (1455 [10.6%] SK vs 1448 [10.5%] APSAC) or among the pre-specified subset presenting within 0-6 h of pain onset and with ST elevation on the electrocardiogram in whom fibrinolytic treatment may have most to offer (861 [10.0%] SK vs 855 [9.9%] APSAC). No significant difference in 6-month survival was apparent overall or in the subset.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:ISIS-3: a randomised comparison of streptokinase vs tissue plasminogen activator vs anistreplase and of aspirin plus heparin vs aspirin alone among 41,299 cases of suspected acute myocardial infarction. ISIS-3 (Third International Study of Infarct Survival) Collaborative Group. 1111 34

The effects of four inotropic agents with differing ancillary properties [a cardiac glycoside (digoxin), a combined alpha- and beta-adrenergic agonist (dobutamine), a beta-adrenergic agonist (prenalterol), and a phosphodiesterase inhibitor (amrinone)] alone and with subsequent addition of isosorbide dinitrate were compared in 48 consecutive acute myocardial infarction patients with radiographic and haemodynamic (pulmonary artery occluded pressure greater than 18 mm Hg) left ventricular failure. All agents with the exception of dobutamine reduced the elevated left heart filling pressure; only digoxin and dobutamine augmented the cardiac stroke volume index. All drugs except digoxin reduced the SVRI; an arteriolar constrictor response was evident 60 min after digoxin and a tachycardia resulted after combined alpha- and beta- and beta-adrenergic stimulations (dobutamine and prenalterol, respectively). The addition of isosorbide dinitrate reversed the inotrope-induced elevations of systemic arterial pressure and resulted in additional reductions in left heart filling pressure. These data suggest that, in the absence of substantial venodilator properties in an inotropic compound, reduction in elevated left heart filling pressure is not achieved with inotropic therapy alone in acute left ventricular failure and combining a venodilator may be haemodynamically advantageous.
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PMID:Modulation of inotropic therapy by venodilation in acute heart failure: a randomised comparison of four inotropic agents, alone and combined with isosorbide dinitrate. 137 84

Streptokinase is the thrombolytic agent most commonly used for the treatment of acute myocardial infarction. We report eight patients who developed late uncommon adverse reactions to streptokinase probably due to immune complex disease. The clinical manifestations included vasculitic rashes, abnormal renal and liver function tests and a syndrome resembling adult respiratory distress syndrome. Major adverse events with streptokinase such as stroke, bleeding and other allergic reactions, have been previously documented but the morbidity related to delayed reactions has not been widely recognised. These reactions produced significant morbidity resulting in prolonged hospital stay and may need to be considered in the decision to use streptokinase.
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PMID:Streptokinase morbidity--more common than previously recognised. 138 52

Epidemiological studies have demonstrated that, compared with the population as a whole, there is increased cardiovascular morbidity and mortality among lower socio-economic groups. To explore determinants of the increased risk within this group, a prospective 6.5 year investigation of a cohort of 416 middle-aged (40.8 +/- 9.6 years) male blue-collar workers was undertaken. In addition to established somatic and behavioural risk factors, psychosocial influences that measured chronic occupational stress in terms of an imbalance between high effort and low reward were assessed. Multivariate logistic regression analysis shows that hypertension (odds ratio (o.r.) 3.85; 95% CI 1.59-9.34), left ventricular hypertrophy (o.r. 3.62; 95% CI 1.06-12.37), hyperlipidaemia (o.r. 2.55; 95% CI 1.08-6.00), status inconsistency (measuring low reward at work) (o.r. 2.86; 95% CI 1.04-7.80) and 'immersion' (measuring high intrinsic effort at work) (o.r. 3.57; 95% CI 1.22-10.47) independently contribute to the prediction of fatal or non-fatal cardiovascular events (acute myocardial infarction, stroke). Expected probabilities of cardiovascular events are clearly elevated if the combined effects of left ventricular hypertrophy and psychosocial risks are analysed. In conclusion, increased incidence of cardiovascular disease among lower socio-economic groups is explained by a co-manifestation of established risk factors including left ventricular hypertrophy (by ECG) and psychosocial factors measuring chronic stress at work.
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PMID:The role of hypertension, left ventricular hypertrophy and psychosocial risks in cardiovascular disease: prospective evidence from blue-collar men. 139 66

Coronary thrombolysis with streptokinase or tissue plasminogen activator is useful for the treatment of acute myocardial infarction in selected patients. This treatment is associated with local hemorrhagic complications and age-related cerebral hemorrhage. Coronary thrombolysis is contraindicated in patients with transient cerebral ischemia and stroke, arterial hypertension, cerebral trauma, cerebral aneurysms, and arteriovenous malformations, because of the risk of cerebral hemorrhage. We report the occurrence of a cerebral hemorrhage related to cerebral amyloid angiopathy in a patient who underwent thrombolysis and treatment with heparin for acute myocardial infarction. Despite normal coagulation parameters, the cerebral hematoma enlarged over 36 hours, as documented by sequential computed tomographic scans, to produce significant mass effect, which prompted surgical evacuation. Histological examination of the resected specimen demonstrated the strong affinity for Congo red and yellow-green birefringence that are characteristic of cerebral amyloid angiopathy. Hemostasis was difficult to achieve, as the divided or disrupted amyloid-laden cortical vessels failed to vasoconstrict, their contractile elements replaced by amyloid beta protein. The patient died of recurrent myocardial ischemia 3 days postoperatively. The incidence of cerebral amyloid angiopathy increases with advancing age. It must be considered as a potential source of cerebral hemorrhage in elderly patients undergoing thrombolysis for cardiac ischemia. Such an occurrence presents a difficult challenge because cardiac function is compromised, the coagulation profile may be altered, the cerebral hematoma is life threatening, and intracranial hemostasis is difficult to achieve.
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PMID:Cerebral hemorrhage from amyloid angiopathy and coronary thrombolysis. 140 40

The introduction of positron emission tomography (PET) as a powerful imaging modality has played a major role in the understanding of the pathophysiological bases for cerebrovascular disorders. PET is the only technique that allows measurement of regional cerebral blood flow, blood volume, oxygen extraction fraction, and oxygen and glucose metabolism with detail and accuracy. Using PET, these physiological parameters can be measured to determine the extent of the disease from the early stages of cerebrovascular disorders to acute cerebral infarction. Significant hemodynamic and metabolic abnormalities are noted in chronic ischemia, but no structural changes are noted on anatomic images. PET studies have shown that in many patients in the early phases (10 to 12 hours) of clinically diagnosed acute stroke, a substantial area of ischemia exists, which, if untreated, will become irreversibly damaged. Similar to the results achieved in patients with acute myocardial infarction, appropriate intervention in patients with cerebrovascular disorders may significantly reduce the extent of injury to the brain. PET also has been useful in predicting functional recovery and monitoring the effects of various therapeutic approaches. Although functional imaging of the brain with single photon emission computed tomography can successfully be used in the investigation of several disorders of the brain, its role in cerebrovascular disorders is quite limited. PET is a unique modality that studies ischemic diseases of the brain, and it potentially could play a significant role in the management of patients with cerebrovascular disease. This will be further realized when aggressive approaches are used routinely in the future.
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PMID:Positron emission tomography in cerebrovascular disorders. 143 68


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