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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A large number of pharmacological trials have been carried out, attempting to reduce the mortality (10-15%) in the year following of an acute myocardial infarction (MI) and/or the recurrence of ischemic events. Thrombolytic therapy and beta-blockade are the only interventions to be associated with a significant decrease in cardiac mortality. Early intervention with intravenous beta-blockers aims at limiting infarct size and at decreasing mortality. The Swedish study using intravenous (15 mg) followed by oral (200 mg/day) metoprolol showed a 36% reduction in mortality after the first week, a benefit persisting after 1 year. The combination of streptokinase and intravenous atenolol is safe and may be beneficial in selected patients. Large-scale controlled multicenter studies have shown that beta-blockers introduced within the first 3 days after acute MI significantly reduce total mortality and/or sudden death in the year following the acute event. Some of these studies demonstrate a reduction in recurrence of MI. The reduction (averaging 25%) in mortality may be explained by the anti-ischemic action of beta-blockers and the prevention of arrhythmia-induced death. Introduced early, beta-blockers may reduce the size of the initial MI as well as subsequent infarction and/or ischemia. Furthermore the antistress action of beta-blockers results in a decrease in free fatty acids, with their untoward effect in acute MI. Antiplatelet aggregation may also play a role. These properties of beta-blocking agents should be utilized in every patient with acute MI in the absence of any major contraindication. Elective indications include patients with hypertension, angina pectoris, and/or ventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Secondary prevention after myocardial infarction: in favor of beta-blockers. 170 16

Chronic arterial hypertension (HT) and left ventricular hypertrophy (LVH) increase the morbidity and mortality of acute myocardial infarction in patients. In this article, we discuss earlier studies from Koyanagi et al. in our laboratory that showed that when animals with chronic HT and LVH (HT-LVH) were subjected to acute coronary artery occlusion (CAO), there was a 3.5-fold increase in mortality and a 35% increase in infarct size expressed as a percent of the area at risk. We subsequently determined the effect of HT-LVH on the wavefront of myocardial infarction. Dogs were made hypertensive using a single-kidney, single-clip model of renovascular hypertension that produced mean arterial blood pressure (BP) = 141 +/- 3 mm Hg and left ventricular:body weight = 5.8 +/- 0.1 g/kg (p less than 0.05 vs. control animals). Conscious animals with HT-LVH and control animals were subjected to 1 or 3 h of CAO. Infarct and risk areas were measured using triphenyltetrazolium chloride (TTC) stain and barium angiography, respectively. The results suggested that the wavefront of infarction was accelerated in animals with HT-LVH. Further studies suggested that the wavefront of myocardial infarction could be markedly retarded by normalizing blood pressure (nitroprusside) 1 h following CAO. Recent studies in an animal model of HT-LVH suggested that electrophysiological abnormalities occur when these animals were subjected to CAO. Sixty-five percent of animals with HT-LVH had sudden death during CAO compared to 27% of the control group. We studied whether chronic beta-adrenergic blockade would reduce mortality associated with CAO in animals with HT-LVH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of coronary artery occlusion in animals with hypertension and left ventricular hypertrophy. 171 84

Left ventricular hypertrophy (LVH), an increase in the muscle mass of the left ventricle, has been identified as a powerful risk factor for future cardiovascular morbidity and mortality. The risk of acute myocardial infarction, congestive heart failure, sudden death, and other cardiovascular events increases six- to eightfold with the presence of LVH. The increase in myocardial mass lowers coronary reserve and enhances cardiac oxygen requirements, gives rise to ventricular ectopy, and impairs left ventricular filling and contractility. Hypertension, obesity, advanced age, valvular heart disease, and other disorders that cause an increase in the hemodynamic burden can lead to LVH. Left ventricular hypertrophy and its sequelae can be reduced by specific antihypertensive therapy but, despite these promising findings, future epidemiological studies are necessary to document the clinical benefits of a reduction of LVH.
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PMID:Left ventricular hypertrophy: an independent risk factor. 172 10

For 30 months, from 1988, some risk factors and the satisfaction of basic needs, such as food, habitation, clothes, transport, health, security, family relation, possibility of affirmation, possibility of creation and cultural needs, were studied in 103 under 55-year-old patients with acute myocardial infarction and unstable angina pectoris. The control group matched the coronary group in age, sex, marital status, education, and working place. A cardiovascular clinical examination and ECG recording were performed in all subjects. In the coronary group also CPK and glucose in serum were recorded several times. Each person estimated the fulfillment of his basic needs from 1 to 5. The family history of coronary heart disease was positive in 43 (41.7%) coronary patients and in 12 (11.6%) control subjects (P less than 0.05). The prevalence of arterial hypertension in the coronary group was 46.6% and of diabetes mellitus 12.6%. In the coronary group 74.7% patients smoked and in the control group 47.5% (P less than 0.01). The mean body index in the coronary group was 27.5 +/- 0.36 and in the control group 27.9 +/- 0.36 (P less than 0.05). The basic needs (food, habitation, clothes, transport, and cultural needs) were given a significantly higher mark in the coronary than in the control group (P less than 0.05). The study has shown significant differences in the presence of classical risk factors between the group of 103 acute coronary patients and the control group. The socio-economic was higher in the coronary than in the control group.
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PMID:[Risk factors and satisfactory living circumstances in 103 patients with acute coronary disease under 50 years of age]. 172 14

It is well known that changes in serum potassium cause ventricular arrhythmias as a result of clearly documented changes in the electrophysiological characteristics of single fibers. Hypopotassemia induced by thiazide and loop diuretics may contribute to the incidence of sudden cardiac death in patients with hypertension and those with congestive heart failure. In addition, hypopotassemia appears to be an independent risk factor for lethal ventricular arrhythmias occurring in the setting of acute myocardial infarction and contributes significantly to arrhythmias associated with starvation and alcoholism. The increase in myocardial extracellular potassium that occurs in the ischemic zone after coronary occlusion is clearly a major factor in the genesis of lethal ventricular arrhythmias that occur in this setting. A decrease in serum magnesium is also believed to be arrhythmogenic, and magnesium depletion is thought to play a role in many of the arrhythmias associated with hypopotassemia. Moreover, the administration of magnesium salts may be effective in the management of life-threatening ventricular arrhythmias. However, definite evidence establishing a causal relation between ventricular arrhythmias and hypomagnesemia or intracellular magnesium depletion is lacking. Changes in intracellular calcium contribute to the arrhythmias associated with acute ischemia and with reperfusion and may be important in the genesis of ventricular tachycardia induced by exercise and by digitalis. Thus, electrolyte and metabolic abnormalities clearly underlie lethal ventricular arrhythmias in a wide variety of clinical situations and should be routinely considered as potential etiologic factors in patients with life-threatening ventricular arrhythmias, particularly those with hypertension and congestive heart failure who are receiving thiazide and loop diuretics.
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PMID:Electrolyte abnormalities underlying lethal and ventricular arrhythmias. 172 8

Stroke is a potentially serious complication of acute myocardial infarction (AMI). In the prethrombolytic era, most strokes were attributed to cerebral embolism. On the basis of available information, the occurrence of stroke in the thrombolytic era appears to be less than in the prethrombolytic era. In the thrombolytic era, the occurrence of various forms of intracranial hemorrhage has increasingly been documented in addition to cerebral embolism, with intriguing features. In general, however, the delineation of specific stroke subtypes has been imprecise and must take into account factors that are unique to this setting. Age is a risk factor for both ischemic and hemorrhagic stroke. Potential risk factors for intracranial hemorrhage include hypertension, dosage of fibrinolytic agents, and prior neurologic disease. Potential causes of intracranial hemorrhage include combined fibrinolytic/adjunctive therapies, various cerebrovascular lesions, and head trauma. Existing data suggest that mortality related to stroke complicating AMI is on the decline as well. More research is needed in order to quantify precisely the occurrence and proportions of stroke subtypes, risk factors, and causes in order to define mechanisms and preventive measures.
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PMID:Ischemic stroke and intracranial hemorrhage following thrombolytic therapy for acute myocardial infarction: a risk-benefit analysis. 172 76

This study compares women and men undergoing coronary artery bypass grafting. Factors before and after coronary surgery were examined to identify variables related to mortality and morbidity. The study population included 465 women and 465 men matched for age (mean age 64.2 years) who underwent first time isolated coronary artery bypass grafting between 1983 and 1988. There were higher incidences of systemic hypertension, diabetes mellitus, postmyocardial infarction angina, thyroid gland disease, arthritis (p less than 0.001 for all), acute myocardial infarction (p = 0.03), congestive heart failure (p = 0.03), and emergency surgery (p = 0.02) in women, whereas more men had peptic ulcer disease (p less than 0.001). The in-hospital death rate was not significantly different (women 4.3% vs men 3.7%). For all subjects, emergency surgery (p less than 0.001), significant left main narrowing (p less than 0.05) and renal disease (p less than 0.001) were related to death, whereas history of myocardial infarction (p less than 0.05) and diabetes (p less than 0.05) were related to death only in men. Age and body surface area were not related to death. After surgery men had a higher incidence of atrial arrhythmia (p less than 0.001), and women had a higher incidence of congestive heart failure (p less than 0.001). Although women did not have a higher mortality rate, the data suggest that women and men do not share all the same predictors of mortality after surgery.
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PMID:Patterns of referral and recovery in women and men undergoing coronary artery bypass grafting. 173 56

Multiple clinical trials have demonstrated that thrombolytic treatment early in the course of acute myocardial infarction significantly reduces mortality. Patients under 75 years of age who have had chest pain for no longer than six hours and who demonstrate ST-segment elevation on electrocardiogram are the best candidates for this therapy. Recent studies suggest that there is little difference in effectiveness among streptokinase, alteplase and anistreplase. However, streptokinase is 10 times less expensive than the other agents and causes fewer intracranial bleeds, the major serious adverse effect of thrombolytic therapy. An advantage of anistreplase is that it can be given in a five-minute bolus injection, compared with a one-hour infusion for streptokinase and a three-hour infusion for alteplase. Thrombolytic therapy is contraindicated in patients with known pregnancy, active internal bleeding, uncontrolled hypertension, aortic dissection, intracranial neoplasm or a history of hemorrhagic stroke. Heparin should be administered with both alteplase and streptokinase. Aspirin, beta blockers, nitrates and lidocaine are useful adjunctive therapies in the setting of an acute myocardial infarction.
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PMID:Thrombolytic therapy in acute myocardial infarction. 173 49

After an acute myocardial infarction a 49 year old man developed late recurrent severe ventricular arrhythmias coincident with transient hypertensive episodes. A phaeochromocytoma was diagnosed on the basis of the urinary concentration of catecholamines and computerised tomography of the adrenal glands. After stabilisation of his cardiac rhythm and blood pressure with alpha and beta adrenergic blockade and anti-arrhythmic treatment the right adrenal gland, which contained the tumour, was successfully resected. The diagnosis of a phaeochromocytoma should be considered when recurrent ventricular arrhythmias are associated with intermittent hypertension after myocardial infarction.
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PMID:Recurrent ventricular arrhythmias complicating myocardial infarction in the presence of phaeochromocytoma. 173 35

Captopril is widely used for congestive heart failure and arterial hypertension. Its main side effects are cough, neutropenia, and renal injury. Liver dysfunction has rarely been described. We present a 71-year-old man with an acute myocardial infarction who developed high fever and progressive disturbance of liver function tests, hepatocellular and cholestatic, after beginning captopril. When other, more likely causes for his condition were ruled out, captopril was discontinued and the fever and liver dysfunction then quickly resolved. We recommend periodic laboratory follow-up in patients treated with angiotensin-converting enzyme inhibitors.
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PMID:[Captopril-induced liver dysfunction]. 175 82


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