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)

Cardiac muscle death caused by coronary artery occlusion is a dynamic process that often takes hours or days. Emergency revascularization (saphenous vein bypass graft (SVBG) during acute myocardial infarction (MI) can interrupt myocardial necrosis, salvage ischemic myocardium and revascularize vessels with obstructive lesions not involved in the MI. In this report we describe a preliminary experimental study of 75 patients in which emergency SVBG was the therapy for acute MI. Group 1, 16 patients, required vasoactive medications and/or intraaortic balloon pumping to maintain their blood pressure preoperatively. There was one operative death and two late deaths. Group 2 consisted of 59 hemodynamically stable patients. There were no deaths. The average preop CPK in group 1 was 892 vs 504 in group 2 (p greater than 0.05). Surgical techniques were routine. The average time from the onset of chest pain that continued to surgery was 6.5 hours. Forty patients were restudied. Post- vs presurgical hemodynamics revealed ejection fraction increased by 34% (p greater than 0.05), left ventricular end-diastolic pressure reduced by 40% (p greater than 0.01). End-systolic and end-diastolic volume reduced by 30% (p greater than 0.05), and 15% (p greater than 0.01), and stroke volume improved 25% (p greater than 0.05). Operative mortality was 1.3% and late mortality 2.8%. These results suggest that cautious continued trial of emergency SVBG in patients with evolving MI is warranted.
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PMID:Emergency coronary artery revascularization: a possible therapy for acute myocardial infarction. 44 42

In 45 patients with brain strokes (thrombosis, embolus, intracerebral haemorrhages) and subarachnoid haemorrhages the CPK activity was determined in the cerebrospinal fluid. In most cases a significant rise was observed in CPK activity in the cerebrospinal fluid as compared to the control group. In two cases the dynamics of CPK activity changes were studied in the cerebrospinal fluid during the stroke. It seems that a significant rise in CPK activity develops in the initial phase of the stroke when the area of nervous tissue softening develops and spreads.
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PMID:[Phosphocreatine kinase activity in the cerebrospinal fluid in different types of stroke]. 72 26

In 100 consecutive patients with acute cerebrovascular accident, due to cerebral thrombosis in 72, cerebral hemorrhage in 12, embolus in 6, and subarachnoid hemorrhage in 10, there were 90 who had electrocardiographic abnormalities during the first three days after admission, compared to 50% in a control group. The patients with cerebrovascular accident had a 7- to 10-fold higher incidence of ST segment depression, prolonged Q-Tc interval and atrial fibrillation, and a 2- to 4-fold higher incidence of T wave inversion, conduction defects, premature ventricular beats and left ventricular hypetrophy. Patients who died had a 2-, 3- and 5-fold higher incidence of electrocardiographic evidence of recent myocardial infarction, atrial fibrillation and conduction defects than those who survived, but these changes occurred in only 5, 21 and 14% of all patients, and other electrocardiographic changes could not be correlated with mortality. During the first three days after admission 29 patients had elevation of serum enzymes which may be derived from cardiac muscle, particularly CPK, which was increased 6-fold, compared to 2-fold increases in HBDH, GOT, and LDH. Only 5 of these patients had electrocardiographic evidence of recent myocardial infarction. Patients with elevated serum CPK had a 2-fold higher incidence of ST segment depression, T wave inversion, conduction defects and atrial fibrillation than those with normal CPK, and a mortality of 66%, compared to 30%. Of 41 patients who died, 49% had elevated serum CPK, compared to 15% of 59 patients who survived. These differences were significant (P less than 0.01). Serum CPK was more frequently helpful than the electrocardiogram in evaluating the extent of cardiac damage and in predicting mortality. Patients with acute cerebrovascular accident should have repeated evaluation of serum CPK and the ECG, and be monitored for arrhythmias.
Stroke
PMID:Electrocardiographic changes and myocardial damage in patients with acute cerebrovascular accidents. 89 40

The results of the present investigation indicate that ISDN infusion following experimental coronary occlusion in anesthetized dogs (1) lowers systemic, cardiac, and pulmonary blood pressures; (2) decreases systemic resistance; (3) has no significant effect on cardiac output, heart rate, and stroke volume; (4) decreases serum CPK levels; and (5) has little effect on blood biochemical parameters. These results suggest that ISDN may have a minimal effect on the ischemic heart by means of a slight decrease in peripheral vascular resistance and systemic blood pressure.
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PMID:The effect of isosorbide dinitrate following experimental coronary occlusion. 94 33

Male and female, arteriosclerotic (breeder) and nonarteriosclerotic (virgin), Sprague-Dawley rats were made severely diabetic with alloxan. Two weeks later experimental animals had both carotid arteries ligated to induce a state of acute cerebral ischemia. After six weeks of cerebral ischemia either with or without severe diabetes the animals were killed. Animals which survived either the acute induction of diabetes or cerebral ischemia did not manifest any new episodes of cerebral ischemia. Subjects with combined diabetes and cerebral ischemia manifested the greatest loss in body weight, adrenal hypertrophy and thymus gland involution, increased levels of serum CPK and SGOT, but decreased SGPT and LDH, hyperglycemia and hypertriglyceridemia, and the most extensive cerebral edema. It is suggested that diabetic rats may have a greater predilection toward cerebrovascular accidents because the diabetic state contributes not only to an exacerbation of atherosclerosis, but also complicates any condition of cerebrovascular ischemia by creating extracerebral edema.
Stroke
PMID:Chronic diabetes followed by chronic cerebral ischemia induced by bilateral carotid artery ligation in arteriosclerotic versus nonarteriosclerotic rats. 117 43

Six patients with Q-wave myocardial infarction in the ECG, two with coronary disease, two with metabolic alterations, one with acute myocarditis and another with ischemic stroke had an improvement of ECG tracings with disappearance of the Q wave. All had normal plasmatic levels of CPK and CKMB. It is believed that metabolic transitory disturbance of the myocardium increases the rest transmembrane potential turning the cell nonresponsive to electrical stimulus and without mechanical activity (inactive electrical zone, not a necrosis zone, which is an anatomo-pathological diagnosis).
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PMID:[The Q wave in the electrocardiogram: necrosis or an electrically inactive area? Myocardial pseudoinfarct]. 134 Nov 85

The calcium-entry blocker isradipine was tested in a closed-chest pig model for chronic myocardial infarction. Ischemia was evoked in anesthetized pigs (25-35 kg) by inflating a catheter balloon in the left anterior descending coronary artery for at least 45 min. Hemodynamic monitoring and signal averaging of X, Y, and Z electrocardiographic leads were performed (150 beats, filtered at 50 Hz). After reperfusion, all animals developed an accelerated idioventricular rhythm and high creatine kinase (CPK) plasma levels. Coronary venous purines and catecholamines increased transiently. Two hours after reperfusion, heart rate was elevated from the initial 87.5 +/- 6.3 to 126 +/- 6.4 beats/min (p less than 0.01) and the pressure-rate product (PRP, an index of oxygen demand) from 9,530 +/- 630 to 11,950 +/- 790 mm Hg/min (p less than 0.05). After 2 weeks, six surviving pigs had a decreased stroke volume (98 +/- 18 versus the initial 124 +/- 14 microliters/kg, p less than 0.05), a prolonged high-frequency signal-averaged QRS duration (81.2 +/- 6.5 versus 65.7 +/- 2.9 ms, initially; p less than 0.05), and ventricular tachycardias (VTs), inducible by programmed electrical stimulation (PES). After the infusion of isradipine (1 microgram/kg/min for 30 min), the cardiac index increased from 92 +/- 14 to 133 +/- 8.7 ml/min.kg (p less than 0.02). Even at a higher heart rate, the PRP dropped from 12,600 +/- 1,900 to 10,560 +/- 1,400 mm Hg/min (p less than 0.05). Sustained monomorphic tachycardias were inducible in five pigs before and in three pigs after isradipine, and no deterioration of the signal-averaged electrocardiogram parameters was found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of isradipine on hemodynamic parameters and ventricular tachycardia in healed myocardial infarction. 168 21

Heat stroke is a medical emergency characterized by sudden loss of consciousness and by failure of the heat-regulating mechanism, as manifested by high fever (usually above 104 degrees F) and cessation of sweating. Fatality rates for patients with heat stroke can vary from 0% to more than 40%. Immediately after heat stroke has occurred or is suspected, aggressive cooling measures should be initiated. This case illustrates a 24-year-old commissioned officer who developed heat stroke while running in PT formation dressed with shorts and a T-shirt. Although this patient was in good shape and the wet bulb was only 74.4 degrees F, he developed the classic symptoms of heat stroke, with a core temperature of 105.9 degrees F. He further developed hepatic and skeletal muscle enzyme abnormalities (SGOT, 4680; CPK, 327; LDH, 821) with hyposphosphatemia (0.8). This patient had no significant risk factors, and after the appropriate treatment, his enzyme abnormalities returned to normal without sequelae. This paper will discuss symptoms, predisposing factors, complications, treatment, and prevention of heat stroke--a topic that is important to all military physicians, especially to those deployed to hot, humid environments.
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PMID:Exertion-induced heat stroke in a military setting. 210 65

In the paper are presented the results of total enzyme activity investigation: GOT, GPT, LDH and CPK, and of the CPK isoenzymes in the cerebrospinal fluid of 148 examinees and in the serum of 67 examinees with an acute stroke, who were treated at the Intensive Care Unit of the Department of Neurology and Institute of Neuropathology, Clinical Medical center "Rebro". The aim was to determine the reliability of the applied methods in the diagnosis of cerebrovascular diseases, particularly in the differential diagnosis of cerebral hemorrhage, ischemia and subarachnoidal hemorrhage. The highest frequency of pathologic findings of the tested enzymes in the whole group of patients with CVA was obtained in the determination of the CPK total activity assessment, then followed the assessments of LDH activity, isoenzyme CPK profile, GOT and finally GPT activity. A larger number of pathologic findings of all mentioned enzymes and CPK isoenzymes was found in the group of patients with ICH. In the patients with ICH and ISI, who survived stroke a higher incidence of normal findings of the total enzymic activities was found, while in those who died from ICH a higher incidence of pathologic findings could not be established. The correlations between the total CPK activity in the serum and in the cerebrospinal fluid does not exist, as well as the correlation between the CPK isoenzyme profile in the serum and CSF.
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PMID:Study of serum and cerebrospinal fluid enzymes in diagnosis and differential diagnosis of cerebrovascular diseases. 229 Apr 71

The spectrum of neurological complications associated with heroin addiction has changed in the past six years because of the progressive knowledge of the neurological complications related to HIV infection. We reviewed 48 heroin addicts with neurological complications and 452 heroin overdose who were seen in the Emergency Unit of our hospital during 1988 and the publications since 1967. Regarding the overdose we present the results of a prospective study leading to determine the causes. We emphasize the relationship with the level of total morphine in serum, instead of conjugate morphine, and with the presence of high levels of benzodiazepines found in the plasma rather than an hypothetic hypersensitivity phenomenon. We resume the neurological complications related with heroin addiction: spongiform leukoencephalopathy, epileptic seizures, stroke, transverse myelopathy and neuromuscular complications such mononeuropathy, plexopathy, acute inflammatory demyelinating polyradiculoneuropathy, rhabdomyolysis, fibrosing myopathy, musculoskeletal syndrome and acute bacterial myopathy. Some of such complications (i.e. transverse myelitis, polyradiculoneuropathy, leucoencephalopathy) must rise the suspicion of an HIV infection. Likewise, in patients assisted for overdosage we believe it's necessary rule out myoglobinuria by means of CPK serum levels and detection of urine hematic pigments without red blood cels in the urine sediment, in order to prevent and treat the renal failure. We report the results of muscular biopsy found in the musculoskeletal syndrome, which are similar to those found in alcoholic myopathy. Finally, we describe the clinical and diagnostic aspects in an unusually neuromuscular complication: the acute bacterial myopathy.
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PMID:[Non-infective neurologic complications associated to heroin use]. 256 83


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