Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

All potent CNS depressant drugs can depress cardiac function in man in a dose-dependent manner. The dose-effect curve is considerably flatter with several drugs (diethyl ether, cyclopropane, fluroxene, isoflurane, and ketamine), presumably from sympathetic nervous-system activation. Potent analgesics and tranquilizers appear to produce less depression, but have been incompletely studied. Neuromuscular blocking drugs and regional anesthesia produce minimal effects on the heart in healthy people. However, not as much is known about diseased man. For instance, nitrous oxide produces more depression in "muscle" function in IHD patients (43), while diazepam (28) and morphine (44) do not adversely affect pump function in this class of patients. Fluroxene (45) is more depressant in VHD patients, but nitrous oxide (46), morphine (30), fetanyl (46), and droperidol-fentanyl (46) seem to have equivalent effects to those seen in health patients. In any given patient, therefore, accurate prediction of the effect of any anesthetic drug on cardiac performance is not possible. Adequate monitoring and careful titration of drug dose offer the safest method of assuring a satisfactory response.
 ...
PMID:Effect of anesthetic drugs on myocardial performance in man. 1 60

Hospital records of patients with asthma admitted to teaching hospitals in Perth, Western Australia between 1976 and 1980 were examined retrospectively to identify characteristics of the illness which were associated with subsequent death. From 5722 admissions there were 195 deaths to December 1982, 186 of whom had records available (cases); 452 of the surviving subjects were used for comparison (controls). There was no difference in age of onset of asthma or cigarette smoking habits between the two groups, but ischaemic heart disease as an associated condition was significantly more frequent in cases. On admission to hospital an arterial PCO2 less than 45 mmHg was more frequent in those who died, but there were no differences in arterial PO2, lowest pH, highest or lowest FEV1 and FVC. Cases more frequently used home nebulisers and were more frequently prescribed corticosteroids, antibiotics and sedatives or tranquilizers prior to admission, corticosteroids and sedatives or tranquilisers during admission and sedatives or tranquilisers on discharge. These results suggest that cases had more severe asthma in that they were more often treated with home nebulisers, corticosteroids and antibiotics, but with the exception of PaCO2 the commonly used measurements of severity of asthma did not identify those at risk of death. The prescription of sedatives or tranquillisers appears to be associated with an increased risk of death in subjects with asthma.
 ...
PMID:Risk factors for death in patients admitted to hospital with asthma: a follow-up study. 175 14

Stroke incidence in Copenhagen, Denmark was recorded in a random population sample of 19,327 persons invited for two health examinations with 5 years' interval from 1976 to 1983. Stroke incidence increased exponentially with age. After adjustment to the age and sex distribution of the Danish population in 1980, the estimated incidence of first stroke was 1.41/1000 women and 2.48/1000 men; the total incidence was 1.94/1000 population. Risk factor analysis was based on the initial examination of 13,088 persons greater than 35 years old without previous stroke who responded to the first invitation, in whom 295 first strokes were subsequently observed. We used the regression model of Cox. However, our use of this model differs from the somewhat automatic procedures normally used to develop prognostic models. Evaluation of the causative effect of a particular risk factor requires that the direction of mutual influences between the factor in question and other risk factors is established/postulated. Among the 16 potential risk factors for stroke we examined, significant effects were found for age, sex, household income, smoking habits, systolic blood pressure, diabetes, plasma cholesterol concentration, ischemic heart disease, and atrial fibrillation. No significant effect could be demonstrated for a positive family history of stroke, years of school education, marital status, alcohol consumption, daily use of tranquilizers, body mass index, or postmenopausal hormone treatment.
 ...
PMID:Stroke incidence and risk factors for stroke in Copenhagen, Denmark. 318 19

This review deals with the following principal concepts: (1) Heart injuries in single severe stress episodes manifested primarily in disturbances of membrane lipid bilayer, sarcolemmal Na, K-pump, and sarcoplasmic Ca-pump with concurrent limited disturbances of the heart energy supply, namely, of the creatine kinase and glycolysis systems. These disturbances cause small focal myocardial lesions and reduce cardiac electrical stability: the fibrillation threshold falls and ectopic activity increases. In repeated stress, this damage, localized mainly in the richly innervated conduction system, accumulates to cause even more pronounced disturbances of electrical stability and severe arrhythmias. (2) Severe stress and beta-adrenergic effects on the heart regularly result in coronary vasodilation and increased coronary blood flow. However, the entire primary complex of stress-induced injuries and disturbances of the heart's electrical stability occurs despite the increased coronary blood flow. Thus, beta-adrenergic stress-induced injuries may indeed develop as primary stress damage to cardiomyocytes without any relation to ischemia. (3) The main factor determining high vulnerability or, on the contrary, resistance of the heart to stress is the state of stress-limiting systems, namely, the opioidergic, GABAergic, cholinergic, adenosinergic, and other systems. Activation of these systems by adaptation to repeated stress or other factors prevents serious injuries to the heart in severe stress. Conversely, genetically determined or acquired dysfunction of these systems predisposes to severe arrhythmias and sudden death. Thus, in stress-induced arrhythmic disease as well as in ischemic heart disease, the main pathogenetic links are outside the heart, but they differ from those observed in ischemia. (4) The clinical picture of stress-induced arrhythmic disease, that is, alterations in electrocardiogram, coronarogram, and patient responses to stress, physical loads, and tranquilizers differ, as do pathologic alterations in the heart. These differences are summarized at the end of this review.
 ...
PMID:Stress-induced arrhythmic disease of the heart--Part I. 808 22