Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

We describe a pulsatile aneurysm in the skin of 16-year-old boy that was found to be a sign of a systemic vascular disease, that is, arterial fibromuscular dysplasia. The patient had aneurysms in the renal, cerebral, coronary, and other arteries; he developed renovascular hypertension and had a cerebrovascular accident and acute myocardial infarction at 17 years of age. This disease has not been previously reported in the dermatologic literature.
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PMID:Aneurysm in the skin: arterial fibromuscular dysplasia. 146 51

Diastolic function is routinely assessed using Doppler-derived left ventricular (LV) filling patterns. Ratios between peak flow velocities during early filling and atrial contraction (E/A) of less than 1 are considered pathologic and diagnostic of impaired relaxation. Myocardial stiffness can normalize the E/A ratio, and thus, in some clinical settings, a normal E/A ratio may identify patients with high filling pressures. LV filling patterns were studied with Doppler echocardiography in 15 healthy subjects and 38 patients with recent acute myocardial infarction. The results were correlated with clinical and hemodynamic variables. E/A ratio less than 1 was found in 14 patients (37%) and in only 1 control subject; E/A ratio greater than 2 found in 5 patients (13%) and in only 1 control subject; 19 patients (50%) had an apparently normal E/A ratio. No correlation was found between LV filling pattern and ejection fraction or presence of diabetes or arterial hypertension. LV end-diastolic pressures were low to normal in patients with an E/A ratio less than 1 and were usually greater than 15 mm Hg in those with normal or abnormally increased (greater than 2) E/A ratios. Thus, an apparently normal E/A ratio in patients after myocardial infarction may identify those with more severe LV diastolic dysfunction and increased LV filling pressure.
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PMID:Doppler echocardiographic patterns of left ventricular filling in patients early after acute myocardial infarction. 151 19

Among 4,720 consecutive hospital survivors from acute myocardial infarction (AMI) treated in 13 coronary care units between July 1981 and August 1983, the estimated prevalence of electrocardiographic left ventricular (LV) hypertrophy was 6.1%. The prevalence of electrocardiographic LV hypertrophy increased with age and was higher in patients with previous myocardial infarction, angina and systemic hypertension. Mean age of patients with electrocardiographic LV hypertrophy was 67.2 vs 61.4 years in counterparts free of electrocardiographic LV hypertrophy. Patients with electrocardiographic LV hypertrophy had a higher rate of congestive heart failure on admission, or developing during their stay in coronary care units. The 1- and 5-year mortality rates were 19.7 and 46.6% among patients with electrocardiographic LV hypertrophy versus 8.7 and 26.2%, respectively (p less than 0.001) in patients without this finding. The covariate-adjusted odds ratio of 1-year mortality was 1.88 for the presence of electrocardiographic LV hypertrophy when age alone was adjusted for, and 1.51 (90% confidence interval, 1.09 to 2.10) when multiple covariate adjustment was undertaken. After multiple covariate adjustment for 5-year mortality after discharge, the relative risk associated with electrocardiographic LV hypertrophy was 1.51 (90% confidence interval, 1.26 to 1.80). The results of the present study showed that the presence of electrocardiographic LV hypertrophy on the discharge electrocardiogram of survivors from AMI is associated with a 1.5-fold increase of short- and long-term mortality. Patients with electrocardiographic LV hypertrophy, potentially at an increased post-discharge risk, may be candidates for early noninvasive testing and more intensive follow-up after recovering from AMI.
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PMID:Long-term prognosis after acute myocardial infarction in patients with left ventricular hypertrophy on the electrocardiogram. SPRINT Study Group. 153 81

Up update of the literature related with the relationship between arterial hypertension and ischemic heart disease is done. The epidermiological aspects, J-curve phenomenon, relationship between arterial hypertension and acute myocardial infarction and the consequences of left ventricular hypertrophy are analysed.
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PMID:[Arterial hypertension and ischemic cardiopathy]. 153 4

The authors report 22 cases of myocardial infarction documented by selective left ventriculography and coronary angiography in women under 45 years of age. The average age in this series was 36 +/- 6.8 years. Two patient groups were identified: Group I (n = 16) with the cardiovascular risk factor of oral contraception (mean age 33.9 +/- 5 years); and Group II (n = 6) comprising older patients (43.8 +/- 1.8 years) with a high prevalence of other risk factors (hyperlipidaemia, hypertension, diabetes). Myocardial infarction tended to be the inaugural event in Group I (9 out of 16 cases, 56.2%) whereas symptoms of effort angina were commonly observed in Group II (5 out of 6 cases, 83.3%). Coronary angiography showed more severe coronary lesions in Group II (score 1.5) than in Group I (score 0.75) in which isolated, single vessel disease mainly affecting the left anterior descending artery or normal coronary angiography was observed. Thrombolytic therapy was performed in 8 patients: percutaneous transluminal angioplasty was performed in 4 patients in the first month with a primary success in 3 cases. Coronary bypass surgery was performed in 1 case. The outcome during follow-up lasting 44.5 +/- 4.2 months was mainly favourable as 15 of the 20 patients had no secondary complications. Nevertheless, 2 patients died in the hospital period (1 from cardiogenic shock and 1 from complications of transluminal coronary angioplasty), 2 patients died less than 1 year after acute myocardial infarction (1 sudden death, 1 cardiogenic shock). Although oral contraception was withdrawn in all cases, many women continued to smoke.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Myocardial infarction in young women: apropos of 22 cases. Pathogenic and prognostic approach]. 155 Apr 34

Drug-induced hypokalaemia is a widespread problem in the elderly that can be caused by many therapeutically useful substances, the most common of which are diuretics. In certain classes of patients (e.g. those with acute myocardial infarction, with congestive heart failure receiving digitalis, or with cirrhosis), iatrogenic hypokalaemia is an established risk factor. In patients with hypertension who have no underlying heart disease or liver disease, the use of diuretics may lead to worsened glucose tolerance and cardiac arrhythmias. There is also evidence for an increased risk of sudden cardiac death.
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PMID:Drug-induced hypokalaemia. A cause for concern. 155 72

Strategies designed to decrease coronary heart disease (CHD) associated morbidity and mortality have focused primarily on established risk factors, including hypercholesterolemia, systemic hypertension, and cigarette smoking. Indeed, primary and secondary intervention trials have provided evidence for cholesterol lowering as an efficient method of CHD risk reduction. To test the hypothesis that serum total cholesterol influences the clinical outcome following acute myocardial infarction, infarct size, left ventricular ejection fraction, infarct-related vessel patency, and in-hospital cardiac events were determined in 106 consecutive patients given thrombolytic therapy within 5 h of symptom onset. Cumulative 48-hour creatine kinase (CK) release, peak CK, and calculated infarct size did not differ significantly between patients with an admitting serum total cholesterol level less than 200 mg/dl (group 1) and those with a cholesterol level greater than 250 mg/dl (group 2). Total cholesterol did not correlate with either cumulative CK release, peak CK, infarct size, vessel patency, or left ventricular ejection fraction. The vessel patency correlated inversely with cumulative CK release (r = -0.27; p = 0.03) and directly with left ventricular ejection fraction (r = 0.24; p = 0.03). The incidence of in-hospital cardiac events including recurrent infarction, congestive heart failure, and death was 6.9, 13.9, and 2.6%, respectively, and did not differ significantly between patient groups. Thus, although serum total cholesterol has been shown to influence CHD incidence, morbidity, and overall mortality, the findings of our study suggest that it does not impact directly on infarct size, left ventricular function, or in-hospital clinical outcome among patients sustaining acute myocardial infarction.
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PMID:Relationship between serum total cholesterol, infarct size, and early clinical outcome following acute myocardial infarction. 155 16

Endothelin is a newly discovered potent vasoconstrictive polypeptide released by endothelial cells in response to various stimuli, including vasoactive peptides such as angiotensin II, adrenaline and vasopressin, and thrombocyte products like transforming beta growth factor and thrombin. Endothelin is believed to exert its main effects locally, in a paracrine or autocrine way. In vascular tissue, endothelin induces longlasting contraction of smooth muscle cells, leading to decreased blood flow, especially in the coronary and renal circulation, together with an increase in systemic blood pressure. It acts also mitogenically in vascular smooth muscle cells. Endothelin stimulates release of aldosterone and catecholamines in non-vascular tissue, and inhibits release of renin. A physiological function of endothelin may be to modulate vascular tone, and increased levels of circulating endothelin are seen after the "cold pressor test". Moreover, plasma endothelin concentration is elevated during acute myocardial infarction, in acute renal failure, in patients with hypertension, and during cardiogenic chock. What role endothelin plays in the development of these conditions, and in other disorders such as vascular spasm and atherosclerosis is uncertain.
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PMID:[The endothelial cell as an endocrine organ--endothelin]. 155 33

In a study of biological risk factors for sudden death in patients with coronary artery disease, 320 patients were, prospectively, recruited and followed-up over two years. None of the patients had heart failure or recent myocardial infarction. The following variables were recorded: previous acute myocardial infarction, hypertension, smoking habits, ventricular arrhythmia; the angiographic variables included: left ventricular ejection fraction, Jenkins' and mean atherosclerotic scores; lipid profile: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoproteins Al and B; hemostatic profile: fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2-antiplasmin, euglobulin clot lysis time and tissue plasminogen activator before and after venous occlusion, tissue plasminogen activator inhibitor, platelet factor 4, beta-thromboglobulin. During the follow-up period, 12 of the patients died suddenly. In these patients, ejection fraction was lower: 49 +/- 16% versus 61 +/- 14% for the other patients (P less than 0.02), fibrinogen higher: 3.9 +/- 0.8 g/l versus 3.5 +/- 0.8 for the living patients (P less than 0.05) and protein C lower: 89 +/- 39% versus 111 +/- 39% (P = 0.06) for the other patients. In multivariate analysis: lower ejection fraction (P less than 0.008), older age (P less than 0.03) and lower protein C (P less than 0.01) were correlated with sudden death. Among the patients with coronary artery disease, the raised fibrinogen and the decreased protein C appeared to be risk factors for sudden cardiac death. These alterations reflected a prothrombotic state which might increase the ischemic risk, due to an acute thrombosis, leading to the fatal ventricular arrhythmia. Determination of these hemostatic variables might be a useful adjunct for assessment of the vital prognosis of patients with coronary artery disease, especially the risk of sudden death in addition to other known clinical, electrocardiographic, hemodynamic risk factors. This would also guide both the instigation of complementary investigations and appropriate therapy in such high risk group of patients.
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PMID:Biological risk factors for sudden death in patients with coronary artery disease and without heart failure. 156 56


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