Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to assess the effects of gallopamil and atenolol administration on left ventricular (LV) relaxation and filling in patients (pts) with acute myocardial infarction (AMI), by pulsed Doppler echocardiography (PDE). Two days after first AMI, 14 pts aged 56 +/- 10 years in Killip class I and treated with thrombolysis were randomized to gallopamil (50 mcg/Kg over 5 min) or atenolol (5 mg over 5 min) IV 10 ml bolus, with a 24 hour time interval, in a cross-over double blind sequence. Four PDE were performed in each patient: at baseline, before gallopamil and atenolol IV bolus, and a 15 min after each bolus. The following Doppler parameters were calculated: early (E) and late (A) peak filling velocities and their ratios (E/A), early (Ei), late (Ai) and total (TVi) diastolic filling time velocity integrals; the ratio between Ei and Ai (Ei/Ai), the peak filling rate normalized to mitral stroke volume (calculated as E/TVi [nPRP]), the percentage of atrial contribution to total diastolic filling (%AC), and the isovolumic relaxation time (nTRIV) normalized to an 800msec RR cycle length. Compared to baseline PDE evaluation, gallopamil administration significantly shortened nTRIV (89 +/- 13 vs 116 +/- 13 msec), improved early LV filling parameters (E: 74.5 +/- 14.0 vs 58.1 +/- 14.6 cm/sec; E/A 1.2 +/- 0.4 vs 0.9 +/- 0.3; Ei: 11.2 +/- 1.8 vs 8.9 +/- 2.0 cm; Ei/Ai: 1.8 +/- 0.6 vs 1.3 +/- 0.6; nPRP: 3.9 +/- 1.0 vs 3.5 +/- 1.0 SV/sec), and reduced %AC (35.6 +/- 8.8 vs 44.6 +/- 10.6). A and Ai were not significantly changed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pharmacological effects on left diastolic ventricular function in acute myocardial infarct: comparison of gallopamil and atenolol]. 181 2

To study past histories of patients who died suddenly, we selected cases from all the summary death certificates in which death occurred within 24 hours from the onset of symptoms spanning 1984 to 1986 in Niigata prefecture with a population of 2.5 million. We then re-examined all information on the death certificates to determine the underlying causes. Sudden deaths due to cardiovascular diseases other than acute myocardial infarction and cerebrovascular accident (OCD) accounted for the largest proportion (51.4%). The proportion of death of unknown etiology increased with the decrease in age in both sexes aged 15 to 54 years, accounting for 67.8% in males and 51.1% in females. The number of cases with histories of diseases related to atherosclerosis (e.g. hypertension, old cerebrovascular accident, etc) increased with age in both sexes, accounting for 38.5% in males and 36.4% in females, both aged 75 years old and over. Except diseases related to atherosclerosis, the past histories accounted for 2.5% or greater were as follows: alcoholism (4.1%), psychiatric disorder (PSY, 2.9%) and valvular heart diseases (VD, 2.6%) in 15-54-year-old males; ischemic heart diseases (IHD, 9.4%), arrhythmia without organic heart diseases (ARR, 2.5%) and VD (2.5%) in 55-74-year-old male; IHD (11.4%), bronchial asthma (3.7%), common cold within one month (CC, 3.6%), cor pulmonale or its related diseases (3.0%) and ARR (2.6%) in male of 75 years old and over; PSY (8.7%), IHD (5.8%), VD (5.1%), pregnancy, delivery or related diseases (4.4%), chronic renal failure (3.6%) and CC (2.9%) in 15-54-year-old females; IHD (10.2%), VD (3.2%) and ARR (2.6%) in 55-74-year-old females; and IHD (11.8%) in females of 75 years old and over. When diseases related to atherosclerosis were included, half of the sudden death cases due to OCD had past histories of underlying cause. As descriptions of past histories are often incomplete, there were probably more cases with past histories. The results of this study indicate that investigation of past histories may aid in elucidating and preventing sudden death.
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PMID:[Past histories of sudden death without specific underlying disease]. 184 23

Thrombolytic therapy has recently been shown to be beneficial in the setting of acute myocardial infarction, and thrombolysis resulting in vascular recanalization has been achieved in several other human disease states, including stroke. Advances in the understanding of the fibrinolytic system have led to the development of several new and distinctive thrombolytic strategies. Animal studies of stroke have been encouraging with regard to arterial recanalization and safety. Clinically, the availability of brain computed tomography has allowed pilot studies to proceed by providing rapid identification of patients with nonhemorrhagic stroke. Arterial recanalization has been demonstrated in patients with ischemic stroke following the administration of any one of several thrombolytic drugs. Placebo-controlled trials have not been completed, and so clinical benefit has not been established. Even though the development of brain hemorrhage has been an infrequent complication, the very high morbidity and mortality have been worrisome. Ironically, thrombolytic therapy holds promise for treatment of subarachnoid hemorrhage and perhaps also for spontaneous intracerebral hemorrhage. Human studies have been limited, but complications have been modest, and clinical outcomes have been encouraging.
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PMID:Thrombolytic therapy for stroke. 185 97

The authors report their experience from 1985 to 1988 with 75 consecutive patients affected by bilateral carotid artery stenosis in whom only one side was surgically treated and the other had a minor (15-45%) asymptomatic carotid stenosis. These patients have been followed for a period ranging from 10 to 50 months (mean follow-up 21 months) by clinical examinations and non-invasive investigations (Doppler CW, Duplex scanner). The non-invasive evaluation included assessment of haemodynamic data and characterisation of plaque morphology (regular vs. irregular or ulcerated surface, homogeneous vs. heterogeneous plaque). During follow-up eight patients died: two (2.6%) from acute myocardial infarction, four from stroke (5.3%), and two (2.6%) from other causes. Twenty-five patients (33.3%) had neurological symptoms related to the unoperated side: and four suffered stroke (5.3%). Twenty-one patients had TIAs (28%) related to the observed side. During follow-up five out of 29 (17.2%) homogeneous and 20 out of 46 (43.4%) heterogeneous plaques progressed (p less than 0.01). With regard to the surface characteristics, nine out of 25 regular plaques progressed and only three patients (12%) had neurological events; 19 out of 34 (55.9%) irregular plaques showed a progression and 14 caused neurological symptoms. Fourteen ulcerated plaques (87.5%) progressed (p less than 0.01). Our experience suggests that the basic trend in the follow-up of patients with bilateral carotid artery disease, is that the contralateral unoperated lesion may evolve and become symptomatic. These symptoms are generally TIAs but five patients (4.3%) suffered from strokes related to the unoperated side, all without warning TIAs.
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PMID:Minor asymptomatic carotid stenosis contralateral to carotid endarterectomy (CEA): our experience. 186 89

Between 1972 and 1988, 145 deaths occurred among 3,126 patients attending the Multiple Sclerosis (MS) Clinics in Vancouver, British Columbia (N = 1,583), and London, Ontario (N = 1,543). We could determine the exact cause of death in 82.1% of cases (119 of 145). Of the 119 patients for whom the cause of death was known, 56 deaths (47.1%) were directly attributed to complications of MS. Of the remaining 63 deaths, 18 (28.6%) were suicides, 19 (30.2%) were due to malignancy, 13 (20.6%) to an acute myocardial infarction, seven (11.1%) to stroke, and the remainder (9.5%) to miscellaneous causes, of which two may have been suicides. The proportion of suicides among MS deaths was 7.5 times that for the age-matched general population, and the proportion of MS deaths from malignancy was 0.67 times that for the age-matched general population. The proportion of deaths due to malignancy and stroke was the same for the MS patients and the age-matched general population.
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PMID:Cause of death in patients attending multiple sclerosis clinics. 153 Jul 15

In a randomized trial of the effects on in-hospital mortality of intravenous urokinase plus heparin versus heparin alone, 2,531 patients with acute myocardial infarction in 89 coronary care units were enrolled for greater than 30 months. Patients admitted within 4 hours of the onset of pain were randomized to receive either intravenous urokinase (a bolus dose of 1 million U repeated after 60 minutes) plus heparin (a bolus dose of 10,000 U followed by 1,000 IU/hour for 48 hours) or heparin alone (infused at the same rate). Complete data were obtained in 2,201 patients (1,128 taking urokinase and 1,073 taking heparin). At 16 days, overall hospital mortality was 8% in the urokinase and 8.3% in the heparin group (p = not significant). Among patients with anterior infarction, mortality was 10.3% in the urokinase and 13.9% in the heparin group (p = 0.09; relative risk = 0.73). The incidence of major bleeding (urokinase 0.44%, heparin 0.37%) as well as the overall incidence of stroke (urokinase 0.35%, heparin 0.20%) was similar in the 2 groups. The rates of major in-hospital cardiac complications (reinfarction, postinfarction angina) were also similar.
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PMID:Comparison of intravenous urokinase plus heparin versus heparin alone in acute myocardial infarction. Urochinasi per via Sistemica nell'Infarto Miocardico (USIM) Collaborative Group. 154 77

Patients with major depression admitted to hospital with acute stroke (n = 44), acute myocardial infarction (n = 25), or acute spinal cord injury (n = 12) were examined for differences in their phenomenological presentation of major depression. Depressed stroke patients were found to have significantly higher scores on the syndrome clusters for generalized anxiety and ideas of reference than depressed cardiac or spinal cord injury patients. In addition, significantly more stroke patients met diagnostic criteria for generalized anxiety disorder compared with the other two groups. Although spinal cord injury patients were younger, more likely to be treated with benzodiazepines, and less likely to be treated with beta-blockers, none of these factors distinguished stroke patients with anxious depression from stroke patients with depression only. These findings are consistent with the hypothesis that the etiology of depression following stroke may be different from that associated with myocardial infarction or spinal cord injury.
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PMID:Phenomenological comparisons of major depression following stroke, myocardial infarction or spinal cord lesions. 188 Mar 12

A retrospective study in 1,314 cases with acute cerebrovascular disease was conducted. The clinical diagnosis included cerebral hemorrhage (CH) 489 cases, cerebral thrombosis (CT) 686 cases, cerebral embolism (CE) 68 cases, and subarachnoid hemorrhage (SAH) 71 cases. Of the 1,314 cases there were 21 patients (1.6%) complicated with acute myocardial infarction during the stage of stroke. The percentage of incidence was 2 cases in CH (0.4%), 13 cases in CT (1.9%), 2 cases in CE (2.9%), and 4 cases in SAH (5%). Based on the detail cases reports the incidence, death rate, diagnosis, and pathogenesis of acute cerebrovascular disease complicated with myocardial infarction were discussed respectively.
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PMID:[Acute cerebrovascular disorders and myocardial infarction]. 188 18

In the Thrombolysis in Myocardial Infarction, Phase II pilot and clinical trial, 908 patients [326 (35.9%) in the pilot study and 582 (64.0%) in the randomized study] were treated with 150 mg recombinant tissue-type plasminogen (rt-PA) activator in combination with heparin and aspirin, and 3,016 patients [64 (2.1%) in the pilot study and 2,952 (97.9%) in the randomized study] were treated with 100 mg rt-PA in combination with heparin and aspirin. Adverse neurological events occurred in 23 patients treated with 150 mg rt-PA (2.5%) [nine cerebral infarctions (1.0%), 12 intracerebral hemorrhages (1.3%), and two subdural hematomas (0.2%)] and in 33 patients treated with 100 mg rt-PA (1.1%) [20 cerebral infarctions (0.7%), 11 intracerebral hemorrhages (0.4%), and two subdural hematomas (0.1%)]. The difference in adverse neurological events observed comparing the two rt-PA regimens was primarily due to a higher frequency of intracerebral bleeding among patients treated with 150 mg rt-PA (1.3% versus 0.4%, p less than 0.01). Patients with recent (within 6 months) histories of stroke were not eligible for the study, and patients with any history of cerebrovascular disease were declared ineligible early in the study. The small number of patients (89, or 2.3%) with any history of neurological disease, intermittent cerebral ischemic attacks, or stroke who were enrolled before the stricter eligibility criteria were imposed or on the basis of incomplete baseline information experienced an increased frequency of intracerebral hemorrhage compared with patients without such histories (3.4% versus 0.5%). Mortality at 6 weeks after presentation among 23 patients who had intracerebral hemorrhage was 47.8%. Intracerebral hemorrhage is a severe but infrequent complication of rt-PA therapy for acute myocardial infarction. The combined frequency of intracerebral hemorrhage, subdural hematoma, and cerebral infarction after treatment with 100 mg rt-PA is comparable to that observed in other trials with thrombolytic agents in acute myocardial infarction.
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PMID:Intracerebral hemorrhage, cerebral infarction, and subdural hematoma after acute myocardial infarction and thrombolytic therapy in the Thrombolysis in Myocardial Infarction Study. Thrombolysis in Myocardial Infarction, Phase II, pilot and clinical trial. 189 64

Recent trials of myocardial reperfusion using single-agent thrombolytic therapy and sequential cardiac catheterization have supported a conservative approach to the patient with acute myocardial infarction. To evaluate combination thrombolytic therapy and the role of a previously untested strategy for the aggressive use of cardiac catheterization, we performed a multicenter clinical trial with a 3 x 2 factorial design in which 575 patients were randomly allocated to one of three drug regimens--tissue-type plasminogen activator (t-PA) (n = 191), urokinase (n = 190), or both (n = 194) - and one of two catheterization strategies--immediate catheterization with angioplasty for failed thrombolysis (n = 287) or deferred predischarge catheterization on days 5-10 (n = 288). Patients with contraindications to thrombolytic therapy, cardiogenic shock, or age of more than 75 years were excluded. Global left ventricular ejection fraction was well preserved and almost identical at predischarge catheterization (54%), regardless of the catheterization or thrombolytic strategy used (p = 0.98). Combination thrombolytic therapy was associated with a less complicated clinical course, most clearly documented by a lower rate of reocclusion (2%) compared with urokinase (7%) and t-PA (12%) (p = 0.04) and a lower rate of recurrent ischemia (25%) compared with urokinase (35%) and t-PA (31%). When a composite clinical end point (e.g., death, stroke, reinfarction, reocclusion, heart failure, or recurrent ischemia) was examined, combination thrombolytic therapy was associated with greater freedom from any adverse event (68%) compared with either single agent (urokinase, 55%; t-PA, 60%) (p = 0.04) and with a less complicated clinical course when the composite clinical end points were ranked according to clinical severity (p = 0.024). Early patency rates were greater with combination therapy, although predischarge patency rates after considering interventions to maintain patency were similar among drug regimens. No difference in bleeding complication rates was observed with any thrombolytic regimen. The aggressive catheterization strategy led to an overall early patency rate of 96% and a predischarge patency rate of 94% compared with a 90% predischarge patency in the conservative strategy (p = 0.065). The aggressive strategy improved regional wall motion in the infarct region (-2.16 SDs/chord) compared with deferred catheterization (-2.49 SDs/chord) (p = 0.004). More patients treated with the aggressive strategy were free from adverse outcomes (67% versus 55% in the conservative strategy, p = 0.004), and the clinical course was less complicated when the adverse outcomes were ranked according to severity (p = 0.016). No significant increase in use of blood products resulted from the aggressive strategy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Evaluation of combination thrombolytic therapy and timing of cardiac catheterization in acute myocardial infarction. Results of thrombolysis and angioplasty in myocardial infarction--phase 5 randomized trial. TAMI Study Group. 202 33


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