Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 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.
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PMID:Effect of anesthetic drugs on myocardial performance in man. 1 60

The possibility that DL-carnitine has a protective effect during myocardial ischemia was evaluated by performing two rapid coronary sinus pacing studies 15 minutes apart in 21 patients with coronary artery disease. Eleven patients received DL-carnitine (20 or 40 mg/kg) before the second pacing study. The treated group had a significant increase in mean heart rate (12.5 beats/min, P less than 0.001), pressure-rate product (1,912 units, P less than 0.01) and pacing duration (3.2 minutes, P less than 0.001) after the administration of carnitine. The treated group also had improvements in percent myocardial lactate extraction (8.8 percent increase, P less than 0.001) and left ventricular end-diastolic pressure (a decrease of 5.3 mm Hg, P less than 0.05). There was significantly less S-T segment depression during the second pacing period in both the untreated and treated groups. The results of this study suggest that in ischemic human hearts with reasonably well preserved left ventricular function, DL-carnitine may improve the tolerance for stress associated with an increase in heart rate and pressure-rate product.
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PMID:Improved pacing tolerance of the ischemic human myocardium after administration of carnitine. 3 61

The influence of therapeutic digitalisation on ST depression due to myocardial ischemia was investigated in 11 patients, average age 53.6 years, with coronary heart disease, compared with the effectiveness of nitroglycerine. Therapeutic digitalis led to an average increase of ischaemic ST depression from -0.53 to -0.73 mV. The mean pulmonary arterial and pulmonary capillary pressure decreased slightly, the frequency of pectanginous attacks increased. Independent of the digitalis effect nitroglycerine had an opposing action on these parameters. In decompensated patients with coronary heart disease (n = 4) both digitalis and nitroglycerine produced a shift of the left ventricular function curve as an expression of improved cardiac action. This could not be observed in patients with compensated ventricular function (n = 7). In sufficient ventricular function digitalis led to a further increase of myocardial ischaemic ST depression. In ventricular insufficiency no uniform behaviour was apparent. ST depression induced by digitalis could be reversibly influenced by nitroglycerine.
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PMID:[The action of nitroglycerine on digitalis induced ST depression in patients with coronary disease (author's transl)]. 10 65

To assess the adaptation of the left ventricle to a chronic pressure overload we used echocardiography to study 18 patients with left ventricular hypertrophy caused by systemic arterial hypertension. Increased values for either posterior wall or interventricular septal thickness or both confirmed the presence of left ventricular hypertrophy in all patients and an increase in the average wall thickness to radius ratio was consistent with the development of concentric hypertrophy. No patient had clinical evidence of ischaemic heart disease. Ejection phase indices of left ventricular performance (mean Vcf, fractional per cent of shortening, normalised posterior wall velocity, and ejection fraction) were within the normal range in the basal state in 16 of the 18 patients. The hypothesis is advanced that patients with concentric left ventricular hypertrophy resulting from systemic arterial hypertension usually have normal left ventricular performance in the basal state because values for wall stress remain within the normal range. We conclude that the hypertrophic response to a chronic increase in systemic arterial pressure does not per se result in depression of the basal inotropic state of the left ventricle.
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PMID:Left ventricular performance in patients with left ventricular hypertrophy caused by systemic arterial hypertension. 14 28

Sixty-two autopsied hearts, with left ventricular hypertrophy (LVH) caused by mitral regurgitation (MR), aortic failure (AR), combined valvular disease (CVD), hypertension (HHD), or ischemia (IHD), and 23 control hearts with normal left ventricles were studied morphologically for analysis of modes of hypertrophy and for ECG-pathology correlation. Basic disorders modify the mode of hypertrophy; that is, elongated AR-type LV makes muscle fiber orientation in the outer layer more vertical, and globular MR-type LV makes it more horizontal than normal. High-voltage QRS correlates with hypertrophy of the outer layer which is often associated with that of the inner layer. ST depression and T changes correspond to relative deterioration of the inner and median layers, respectively.
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PMID:Histopathological study of hypertrophied myocardium of known etiologies with special reference to correlation of ECG changes. 14 36

In two patients with primary Type V hyperlipoproteinemia with typical clinical features including recurrent bouts of abdominal pain a myocardial infarction was diagnosed. In both cases coronary angiography revealed a severe three vessel disease. The case reports demonstrate that the incidence of ischemic heart disease in patients with Type V hyperlipoproteinemia is higher than reported in the literature. In each case of severe abdominal pain, even in younger Type V patients, a myocardial infarction has to be excluded, In both patients a selective depression in the activity of lipoprotein lipase was found. The possible pathogenetic implication of this finding will be discussed.
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PMID:[Coronary heart disease in patients with primary type V hyperlipoproteinemia (author's transl)]. 20 63

One hundred and twenty-five consecutive patients being submitted for coronary cinearteriography were subjected to preliminary graded exercise testing using a Quinton treadmill and ECG data computer. Patients with disease of the left main coronary artery are at particular risk during coronary arteriography and it was hoped that exercise testing might identify these patients. This hope was not realised. A satisfactory end point to the exercise test was either the attainment of 85% of the maximal heart rate assessed for age, or ST segment depression greater than 2 mm. Exercise induced angina also formed an end point to the test and was considered a positive result. Results were determined by McHenry's discriminant analysis. The sensitivity of the exercise test was 66, 88 and 92% for one, two and three vessel disease respectively. Specificity was at least 83%. Exercise induced ST segment elevation occurred in four patients all of whom had previous extensive anterior wall infarction. Exercise testing is without risk in patients with ischaemic heart disease provided well defined precautions are taken.
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PMID:The correlation of the computer quantitated treadmill exercise electrocardiogram with cinearteriographic assessment of coronary artery disease. 28 92

The diagnostic performance of automatic analysis of the exercise electrocardiogram in detecting ischaemic heart disease was studied in 147 patients with angiographically documented coronary disease. The results were compared with the results of visual analysis of the same recordings. Using a bicycle ergometer we tried to reach at least 90 per cent of the predicted maximal heart rate of the patient. Two bipolar thoracic leads (CM5, CC5) were used. In the visual analysis the criterion of the so-called ischaemic ST segment was applied. For the automatic analysis the population was divided into a learning group (N=87) and a testing group (N=60). In the learning group first critical values were computed for different ST measurements that provided optimal separation between patients with (CAG POS.) and without (CAG. NEG.) significant coronary stenoses as revealed by coronary arteriography. These critical values were kept unchanged when applied to the testing group. With respect to the visual method an increase of the sensitivity by 0-45 and 0-36 was obtained by the automatic analysis in the learning and testing group, respectively. The best separation between CAG. POS. and CAG. NEG. group was reached using a criterion consisting of a linear combination of the slope of the initial part of the ST segment and the ST depression; the sensitivity being 0-70 and 0-60, respectively, in the learning and testing group. Using a criterion based on the area between the baseline and the ST segment (the SX integral) these values were 0-42 and 0-49, respectively. All specificities were kept to at least 0-90.
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PMID:Clinical value of quantitative analysis of ST slope during exercise. 31 13

Suspecting that platelet thromboemboli could play a role in the pathogenesis of myocardial ischemia, we did a random-order, double-blind, crossover study of the effect of the platelet aggregation inhibitor, aspirin, on treadmill exercise-induced angina in 13 men with coronary artery disease. Although collagen-induced platelet aggregation and the second phase of adenosine diphosphate (ADP)-induced platelet aggregation were significantly decreased and the rate of disaggregation of ADP-induced platelet aggregates was significantly increased after 650 mg aspirin in buffered solution, there was no delay in onset of exercise-induced angina, change in heart rate-blood pressure product at onset of angina, or change in S-T segment depression at onset of angina. Regardless of whether the patients had received placebo or aspirin on the preceding day, treadmill exercise until angina was followed by no changes in platelet aggregation or disaggregation, platelet count in blood or platelet-rich plasma, or of the plasma concentration of nonesterified fatty acids.
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PMID:Effect of aspirin on exercise-induced angina. 34 92

Therapeutic doses of digitalis may give rise to depressions and abnormities of the ST segment. In coronary patients this is occasionally also associated with anginal complaints. In 7 patients the ST segment was investigated at rest and under increasing stress by atrial frequency without and with digitalis at increasing therapeutic dosage. In all patients a glycoside-induced, linearly intensifying depression of the ST segment was demonstrated as a regular and dose-dependent pattern the onset of which was already recognizable at an average effective level of 0,59 mg digoxin. The opinion is held that glycoside-induced ST depressions in the ECG are not in general of insignificant nature but may be the reflection of myocardial ischemia.
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PMID:[Behaviour of the ST segment under stress by atrial frequency and digitalis in latent coronary insufficiency (author's transl)]. 40 33


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