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

Many studies have demonstrated fairly high incidence of supraventricular arrhythmias after coronary artery bypass surgery, and have tried to identify preoperative, operative and postoperative factors related to their appearance. The present paper analysed 186 patients submitted to coronary artery bypass and reported a incidence of atrial fibrillation of 6.04% (11 cases). The male sex was dominant (81.2%) with ages varying from 49 to 73 (mean 54.58) years. The preoperative incidence of diabetes, smoking and systemic hypertension were, respectively, 18.2%, 54.51% and 36.4%. The mean number of vessels bypassed was 2.42 +/- 1.19 and the left circumflex artery was involved in 81.20% of these cases. Cardiopulmonary bypass time was 100 +/- 39.6 min and ischemic arrest time of 79.6 +/- 37.7 min. Single double stage cannulae for venous drainage were used in 45.5% of the patients and ventricular fibrillation and cardiac overdistention occurred in 63.60% immediately after CPB. Atrial fibrillation presented around 1.66 +/- 2.17 days in the postoperative period and 45.5% of the patients had more than one distinct episode of the arrhythmia. Treatment constituted of cardioversion in 25%, atenolol oral in 18.75% and digitalis associated to quinidine in 56.25%. These numbers permit us to suggest that some of the above factors may contribute to the genesis of arrhythmias, such as single double stage cannulation for venous drainage, inadequate myocardial protection, overdistention and cardiac fibrillation and, mainly, the presence of proximal circumflex artery obstructions responsible for atrial ischemia before and during surgery.
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PMID:[Postoperative atrial fibrillation in myocardial revascularization]. 281 36

Cardiac hypertrophy and hypertension are major elements in sudden cardiac death in patients with coronary artery disease. To investigate in animals the hypothesis that left ventricular hypertrophy (LVH) and/or hypertension increase the incidence of severe ventricular arrhythmias, we have undertaken a 30 min period of coronary artery ligation in anaesthetized spontaneously hypertensive rats (SHR), normotensive (NT) Wistar Kyoto (WKY) and Wistar (W) rats. Mean systolic blood pressure (SBP) was 190 +/- 4 mmHg in SHR vs 123 +/- 5 mmHg in WKY and 116 +/- 4 mmHg in W (p less than 0.001). LVH index was 2.81 +/- 0.04 in SHR vs 196 +/- 0.03 in WKY and 1.65 +/- 0.05 in W (p less than 0.01). Incidence (IVF) and duration (DVF) of ventricular fibrillation were significantly more elevated in SHR than in NT rats. IVF was 100 p. 100 in SHR vs 36 p. 100 in WKY and 27 p. 100 in W (p less than 0.001); DVF was 61 +/- 17 s in SHR vs 6 +/- 6 s in WKY and W (p less than 0.001). In addition the calcium channel blocker nicardipine (N) has been administered orally to SHR either chronically during eight weeks (20 mg/kg-1 per os twice daily) or acutely as a single dose of 20 mg/kg. After long term treatment (LT) with N the LVH index and SBP were significantly reduced when compared to vehicle treated (VT) SHR; whereas a single administration of N (AT) only decreased SBP without affecting LVH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Arterial hypertension, myocardial hypertrophy and disorders of cardiac rhythm induced by ligation of the left coronary artery in the rat]. 295 34

Cardiac hypertrophy (CH) and hypertension (HT) are major determinants of sudden cardiac death in patients with coronary artery disease. To investigate the hypothesis that CH and HT increase the incidence of severe ventricular arrhythmias in an animal model, we performed a 30-min period of coronary artery ligation in anesthetized spontaneously hypertensive rats (SHR), normotensive Wistar Kyoto (WKY) and Wistar (W) rats. The incidence and duration of ventricular fibrillation resulting from coronary artery occlusion were significantly (p less than 0.01) increased in hypertensive rats compared to normotensive animals. The calcium entry blocker nicardipine was administered orally to SHR either chronically for 8 weeks (20 mg.kg-1 twice daily) or acutely as a single dose of 20 mg.kg-1. After long-term treatment with nicardipine, left ventricular hypertrophy index and systolic blood pressure were significantly (p less than 0.001) reduced when compared to vehicle-treated SHR, whereas a single administration of nicardipine only decreased blood pressure without affecting cardiac mass. In the long-term nicardipine-treated SHR group, acute coronary artery ligation induced significantly less ventricular fibrillation (p less than 0.05) and mortality (p less than 0.001) than in acutely nicardipine-treated or untreated SHR groups. In conclusion, the data suggest that the severity and incidence of lethal ventricular arrhythmias are more elevated in hypertensive than in normotensive rats and this may be related to the myocardial hypertrophic state.
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PMID:Influence of spontaneous hypertension and cardiac hypertrophy on the severity of ischemic arrhythmias in the rat. 297 94

Verapamil has been established as the drug of choice in the treatment of supraventricular dysrhythmias and is recognized as useful in the treatment of ischemic heart disease and hypertension. However, verapamil has not generally been considered helpful in the treatment of ventricular dysrhythmias. Five cases are reported in which verapamil was used to terminate a cycle of supraventricular tachycardia-mediated recurrent ventricular fibrillation that could not be suppressed by conventional antidysrhythmics such as lidocaine, procainamide, and bretylium, Proposed mechanisms of verapamil's beneficial effect in this usually fatal situation include (1) a reduction in oxygen consumption related to the reduction in heart rate, thereby raising the ventricular fibrillation threshold; (2) direct anti-ischemic effect; and (3) a direct antidysrhythmic effect. These proposed mechanisms are substantiated by clinical studies. On the basis of this observation, it is recommended that in a situation of supraventricular tachycardia-mediated recurrent ventricular fibrillation that cannot be terminated by conventional antidysrhythmics, the administration of verapamil should be considered.
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PMID:Terminating SVT-mediated recurrent ventricular fibrillation with verapamil. 317 Nov 18

Data on the 2,008 patients in the Swedish Co-operative Study from 1969 were compared with 773 consecutive cases with definite myocardial infarction (MI) admitted to the coronary care unit (CCU) of Danderyd Hospital in Stockholm 1984-85. We found a significant decrease in hospital mortality from 26.6% to 12.9% despite the admission of older patients to our CCU. Mean age for men was 63.8 vs. 65.6 years and for women, 69.8 vs. 72.3. The incidence of previous hypertension and diabetes was higher and the incidence of heart failure and angina lower in 1984-85. No differences were noted as regards the incidence of ventricular fibrillation, atrial fibrillation and AV-block III in the acute phase despite a much more frequent use of antiarrhythmics in 1969 (33% vs. 4%). A decreased use of cardiac glucosides was also noted (34% vs. 16%). Asystole, however, was noted in 10% of the patients in 1969 compared with 3% in our patients. beta-Adrenergic blockers were not used in 1969 but commonly given in 1984-85 (67%), also in those with heart failure (54%). Delay between onset of symptoms and admission was longer in 1969, 47% being admitted within 6 hours compared with 75% in 1984-85. In conclusion, our study shows a marked change in the use of various cardiac drugs in the treatment of MI. Differences between the populations as regards mortality and different clinical findings are more difficult to evaluate and may also be explained by change in the selection of patients treated in the CCU.
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PMID:Trends in coronary care. A retrospective study of patients with myocardial infarction treated in coronary care units. 320 63

A 52-year-old apparently healthy, normotensive woman who presented for elective cholecystectomy experienced intra-operative hypertension and tachycardia, which were controlled by propranolol. Oesophageal temperature increased, there was a metabolic and respiratory acidosis with hypoxaemia, and malignant hyperthermia was diagnosed. Severe cardiogenic pulmonary oedema ensued, and was treated with intravenous glyceryl trinitrate. Ventricular fibrillation caused cardiac arrest, and this was treated successfully. Postoperatively a phaeochromocytoma was discovered, and removed at a subsequent operation. The case illustrates the similarities in presentation of malignant hyperthermia and phaeochromocytoma, and the possibility that misdiagnosis may exacerbate the crisis.
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PMID:Phaeochromocytoma--a presentation mimicking malignant hyperthermia. 323 80

Severe acute thallium poisoning in a young man is described. He presented with transient loss of consciousness and paraesthesiae of finger tips and lips, with a blood thallium concentration of 5750 micrograms/l (levels above 200 micrograms/l are toxic). He rapidly lost limb sensation and power and later required temporary mechanical ventilation and nasogastric feeding. The neurological sequelae one year afterwards are a flaccid paraparesis, cerebellar ataxia and mental impairment. Immediate cardiovascular complications included hypertension, sinus tachycardia, ECG abnormalities and an episode of ventricular fibrillation. We were able to assess the relative merits of different methods advocated for enhancing thallium excretion. Oral Prussian blue, forced diuresis and haemodialysis were found to be the most effective: 2000 mg of thallium were eliminated over 20 days, 820 mg over 46 days and 225 mg over 25 days respectively by these methods. Haemofiltration was ineffective. Diethyldithiocarbamate, a chelating agent, brought about a rise in serum thallium concentration accompanied by clinical deterioration and its use should be abandoned.
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PMID:Clinical features and therapy of acute thallium poisoning. 327 37

An experimental model was designed to study hemodynamic and left ventricular functional changes in the course of and after brain death in 13 mongrel dogs. Brain death was induced by creating intracranial hypertension by inflating a balloon inserted into the subdural space. Hemodynamic parameters and left ventricular systolic function as assessed by echocardiography were measured before and during intracranial hypertension and 30 min and 1, 2, 3, 5 and 8 hrs after brain death. During intracranial hypertension, heart rate, systemic and pulmonary blood pressures, cardiac output and systemic vascular resistance raised significantly. After brain death, all parameters decreased rapidly and significantly, and then stabilized. On comparison with values obtained before intracranial hypertension, systemic blood pressure decreased markedly following brain death, while no marked change was noted in cardiac output. This result is attributable to a marked reduction in peripheral vascular resistance following the induction of intracranial hypertension. The left ventricular end-diastolic and end-systolic diameters did not change; consequently, fractional shortening did not change, either. The Weissler's index improved after brain death, reflecting a marked reduction in systemic vascular resistance. This indicates limited usefulness of afterload-dependent cardiac indices. At the agonal period of brain death, three of 13 dogs died because of ventricular fibrillation or a marked decline in systemic blood pressure. Within five to eight hours after brain death, seven dogs died because of intractable acidosis. These results represent the specific hemodynamic features occurring after brain death. It is thought that recognition of these features is useful in managing cases of brain death and in selecting donors for heart transplants.
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PMID:[Effect of brain death on hemodynamics and cardiac function: an experimental study]. 350 5

The epidemiology and etiology, pathophysiology, diagnosis, clinical presentation, complications, and treatment of acute myocardial infarction (AMI) are reviewed. Major risk factors for AMI include age, sex (men greater than women), family history, race, hyperlipidemia, hypertension, cigarette smoking, diabetes mellitus, and diet. AMI occurs when there is a prolonged decrease in oxygen supply to the myocardium caused by coronary thrombosis or coronary vascular spasm. Traditional drug treatment of uncomplicated AMI includes oxygen, laxatives, and analgesics. For analgesia, narcotic agonists are generally preferred, although intravenous nitroglycerin is of value for both reducing infarct size and relieving pain. Fibrinolytic therapy is also indicated in these patients. Low-dose heparin should be initiated on admission to the hospital. Beta-adrenergic blocking agents have proven useful in reducing the incidence of ventricular fibrillation and sudden death. Antiplatelet agents may also be used to decrease long-term mortality. Recent studies have focused on reduction of infarct size using agents such as beta blockers, calcium-channel blockers, nitroglycerin, and thrombolytics. Revascularization procedures are required in some patients to re-establish adequate coronary perfusion. Most patients who survive AMI initially have a relatively uncomplicated clinical course. An increasing number of therapeutic interventions are available for acute and chronic treatment of AMI.
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PMID:Current concepts in clinical therapeutics: acute myocardial infarction. 352 26

The incidence of major ECG changes, particularly ventricular fibrillation, was evaluated in rabbits during prolonged, selective right coronary injection of sodium/meglumine ioxaglate (Hexabrix 160) and iohexol (Omnipaque 140), two isotonic contrast media. The anesthetized animals (n = 12) per test solution) each received 1.5 ml of contrast material, delivered at a rate of 3 ml/minute. Both contrast media caused major ECG changes, which were reversible within seconds after administration. No fibrillation occurred with ioxaglate, but ventricular fibrillation was seen in seven animals given iohexol. There was a significant difference in the incidence of ventricular fibrillation between the contrast media (P less than .01). Both test solutions induced transient, more or less marked bradycardia, but without significant differences. The intracoronary injections produced similar decreases in blood pressure for both contrast agents. Reactive hypertension was observed only in those animals in which an episode of fibrillation occurred with iohexol. The causes underlying these effects are analyzed for both contrast agents.
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PMID:Incidence of ventricular fibrillation during coronary arteriography in the rabbit. A comparative study of isotonic ioxaglate and iohexol. 355 82


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