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)

As many as 24 patients suffering from essential hypertension (EH) were examined. The patients were subjected to Holter ECG monitoring, echocardiography, coronary angiography, exercise scintigraphy of the myocardium with transesophageal pacing of the atria and the dipyridamole test. The patients manifested defects of thallium accumulation during exercise scintigraphy of the myocardium. They were transitory defects of accumulation with clearance impairment recorded in EH patients with atherosclerosis of the coronary arteries; transitory defects of accumulation without clearance impairment recorded in EH patients with the angiographically unchanged coronary arteries. In Holter ECG monitoring, the patients with a silent depression of the ST segment demonstrated transitory defects of thallium accumulation by the myocardium in all the cases during exercise scintigraphy of the myocardium.
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PMID:[Hypertension and "silent" myocardial ischemia. I. The results of stress scintigraphy of the myocardium in patients]. 144 Mar 20

Episodes of ST depression are closely related to transient decreases in regional myocardial perfusion during physical or mental stress. At the onset of these events, there is transient constriction of atherosclerotic stenoses, with an increase in myocardial demand as reflected by increases in heart rate and blood pressure. Recent research has shown that normal epicardial coronary arteries respond to these provocations and to increasing blood flow with progressive vasodilation. In contrast, atherosclerotic vessels lose this ability to dilate and may show paradoxical constriction. This abnormal constriction parallels the response of the arteries to acetylcholine, which can be used to assess the ability of the coronary endothelium to regulate vasodilation. The loss of endothelium-dependent vasodilation appears to be an important functional manifestation of coronary atherosclerosis and a potential triggering mechanism for transient ischemia. Dysfunctional endothelium may also result in a procoagulant surface, with cell adherence and local thrombus formation. Restoration of normal endothelial function is likely to emerge as an important therapeutic objective in the management of myocardial ischemia and coronary atherosclerosis.
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PMID:New insights into the management of myocardial ischemia. 144 5

Holter monitoring was performed in 61 patients with essential hypertension. Painless, silent ST segment depression was found in 34 patients. Exercise myocardial scintigraphy indicated the occurrence of transient perfusion defects without abnormal clearance (Group 1) and those with abnormal clearance (Group 2). The patients from Group 1 showed more severe myocardial hypertrophy, higher platelet aggregation, coronary atherosclerosis was detected in 1 case. The patients from Group 2 exhibited less myocardial hypertrophy, lower platelet aggregation. Coronary atherosclerosis was revealed in 4 cases. The patients from the two groups had elevated plasma norepinephrine levels at the onset of silent myocardial ischemia.
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PMID:[Silent myocardial ischemia in patients with essential hypertension]. 152 31

To investigate the significance of precordial ST-segment depression in acute inferior myocardial infarction, we compared the Gensini score of coronary artery stenosis between 2 groups of patients with and without precordial ST-segment depression. Group I consisted of 28 patients who showed ST-segment depression on admission (greater than or equal to 1 mm in V2-V6) and Group II (n = 16) those without ST-segment depression (less than 1 mm). The Gensini score of the coronary arteries (56 +/- 29 vs. 28 +/- 18; p less than 0.001), the partial score of the infarction-related artery (29 +/- 16 vs. 17 +/- 11; p less than 0.01) and of the infarction-nonrelated artery (27 +/- 24 vs. 11 +/- 12; p less than 0.02) were significantly higher in Group I than in Group II. The Killip score (greater than or equal to II) (34% vs. 6%; p less than 0.05), frequency of arrhythmias (75% vs. 38%; p less than 0.02) and peak CK value (3,676 +/- 2,290 vs. 1,818 +/- 1,153 IU/L; p less than 0.005) were higher in Group I than in Group II. Four patients in Group I died following admission, while no patient died in Group II (N.S.). Autopsy findings from the 4 Group I patients revealed fresh extensive inferior infarction and healed diffuse subendocardial infarction which could not be predicted from electrocardiograms. All patients who survived the acute stage performed treadmill exercise testing and 22 patients underwent exercise thallium-201 single photon emission computer tomography (SPECT). On treadmill exercise test, there was no significant difference between the 2 groups in the frequency of angina pectoris and ST-segment depression. On SPECT, the perfusion defect area under 55% of maximum uptake at the redistribution phase was 45.8 +/- 19.6 cm2 in Group I (n = 14) and 34.7 +/- 21.3 cm2 in Group II (n = 8; N.S.). In conclusion, precordial ST-segment depression in acute inferior myocardial infarction suggested advanced atherosclerosis in both the infarction-related and nonrelated coronary arteries, indicating a larger infarct size.
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PMID:Higher Gensini score of coronary arteries in acute inferior myocardial infarction with precordial ST-segment depression. 157 78

Many studies of age-related cognitive decline have failed to distinguish between usual and successful aging. Although some degree of cognitive impairment is associated with aging, when one looks at average performance, there is great variability among individuals, with many showing little or no deleterious effects of aging on intellectual abilities. Many of the risk factors for dementia and for conditions associated with cognitive impairments can be treated or controlled. Among the preventable causes of cognitive decline are the following: AIDS, Alcohol and drug abuse, Cerebrovascular disease, Exposure to organic solvents or lead, Head trauma, Overmedication, Syphilis. Other conditions that may cause cognitive decline can be controlled or treated: Atherosclerosis, Depression, Diabetes, Emphysema, High blood pressure, Obesity, Sleep disorders, Thyroid dysfunction. In addition, it may be possible to enhance the cognitive performance of even healthy elderly people through changes in diet and lifestyle. Recent data raise the possibility that improved prenatal and perinatal care and greater access to educational opportunities may result in a decreased incidence of dementia in future generations of older adults. Although they are rapidly becoming more numerous, the efficacy of cognitive training programs in preventing or slowing cognitive decline has not yet been demonstrated. Nevertheless, such programs may ameliorate cognitive impairment by reducing the psychiatric disabilities associated with anxiety and depression. The general principle underlying these strategies for limiting cognitive impairment with age is to maximize brain reserve and minimize brain damage.
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PMID:Preventing cognitive decline. 157 76

Atherosclerosis was induced in male mongrel rabbits with a high-fat diet and the influence of essential phospholipids (EPL) on plaque formation, parameters of lipid metabolism and immunological functions was studied. When EPL were added to the high-fat diet there was a significant reduction in the area of atherosclerotic involvement of the aorta. The serum concentration of lipids decreased, often to normal values, and cholesterol esterified with polyunsaturated fatty acids appeared. Normalization of the malonyldialdehyde level in plasma was accompanied by a decrease in the concentration of ascorbate free radicals in blood and liver. The high-fat diet caused a depression of both non-specific and specific immune functions studied. With EPL in the diet the tests showed near normal or normal values. It is inferred from these results that a normal state of the immune system is important for preventing the progress of atherosclerotic changes. This is discussed with reference to the role of some immune cells in the metabolism of lipids and to participation of essential phospholipids in plasma membrane functions.
Atherosclerosis 1992 Mar
PMID:Essential phospholipids modify immunological functions and reduce experimental atherosclerosis in rabbits. 159 5

The aim of this study was to evaluate the efficacy and possibly the mechanism of action of gallopamil and diltiazem in a double-blind crossover trial in patients with effort ischaemia. Twenty male patients (mean age 57 +/- 6 years) with documented coronary atherosclerosis and exercise-induced ischaemia (ST depression greater than or equal to 0.15 mV) completed the study, which consisted of four 7 day periods. At the end of each period a multistage bicycle exercise stress test was performed under placebo (first and third periods) and randomly under gallopamil (50 mg t.i.d.) or diltiazem (90 mg t.i.d.) in the second and fourth periods. Both drugs significantly increased time to ischaemia (0.15 mV ST depression) as compared to placebo, from 7.9 +/- 1.7 min to 8.9 +/- 1.1 min (diltiazem) and 9.1 +/- 1.6 min (gallopamil) with no significant difference between the two drugs, and reduced the maximal extent of ST shift from 0.18 +/- 0.08 mV to 0.13 +/- 0.04 mV (diltiazem) and 0.12 +/- 0.05 mV (gallopamil). Analysis of the results from the whole population showed that the beneficial effect did not appear to be related to any specific parameter. Individual analysis showed that 13/20 patients under gallopamil and 13/20 under diltiazem increased time to ischaemia, while this was unchanged or reduced in the remainder. A positive correlation between changes in time to ischaemia and changes in rate x pressure product at ischaemia was found in both those administered gallopamil (R 0.80, P less than 0.01) and diltiazem (R 0.65, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gallopamil and diltiazem: a double-blind, randomized, cross-over trial in effort ischaemia. 159 29

The aim of this study was to determine the significance of the "coronary factor" in patients with essential hypertension (EH). Electrocardiogram Holter monitoring was performed in 61 patients with EH stage II (according to the World Health Organization criteria). Silent, ie, painless ST-segment depression, was found in 34 patients on whom echocardiography, a treadmill test, and transesophageal pacing were performed. In 21 patients with EH and silent ischemia, the examination included 201Tl stress scintigraphy, coronary angiography, and a platelet aggregation test. In 15 patients, catecholamines and beta-endorphins were obtained in blood samples during silent ischemia. 201Tl scintigraphy showed transient defects of perfusion without clearance abnormalities (group I) and with clearance abnormalities (group II). The patients in group I had more severe left ventricular hypertrophy (LVH) and a significantly higher platelet aggregation response to 0.5 mumol/L adenosine diphosphate; one patient in this group had coronary atherosclerosis. LVH and the platelet aggregation response was less pronounced in the patients in group II, but atherosclerotic lesions of a coronary artery were observed in four patients. In both groups, norepinephrine and beta-endorphin levels were increased during silent episodes of ischemia. The results suggest that there are different pathogenetic mechanisms of coronary insufficiency in patients with EH, a hypertensive heart, and silent ischemia.
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PMID:Silent myocardial ischemia in patients with essential hypertension. 163 37

Calcium antagonists retard the development of atherosclerosis in cholesterol-fed rabbits and modestly enhance regression after their return to a normal diet. Proliferative lesions following endothelial damage (from, for example, balloon catheter, electrical stimulation) are also diminished. Many mechanisms for these effects have been proposed and their relative importance is not yet clear. However, changes in blood lipid levels do not play an important role. Only a few investigations into how atherosclerosis affects the hemodynamic actions of calcium antagonists have been carried out. Thus, the effects of isradipine were compared in atherosclerotic and normal rabbits. Isradipine increased heart rate and cardiac output less in atherosclerotic rabbits than in normal ones while having no effect on the surface electrocardiogram (ECG). In contrast, the arteriolar vasodilator, dihydralazine, induced ST-segment depression with similar falls in blood pressure, partly explainable by reflex tachycardia and intramyocardial maldistribution of coronary blood flow. Flow to the brain increased with isradipine and decreased with dihydralazine. In atherosclerotic animals, the pressor effects of norepinephrine, phenylephrine, and angiotensin II (Ang II) were amplified. Isradipine partly corrected this enhanced responsiveness. Calcium antagonists thus elicit beneficial hemodynamic and antivasoconstrictor effects in atherosclerotic experimental animals, in addition to having a long-term prophylactic antiatherosclerotic action.
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PMID:Hemodynamic, antivasoconstrictor, and antiatherosclerotic effects of calcium antagonists in animal models of atherosclerosis. 169 7

The maximal P-wave duration in all time-aligned leads, and the maximal P-wave amplitude in leads V5 and V6 were measured on a 12-lead, signal-averaged electrocardiogram during the recovery period of an exercise stress test (EST). The study group consisted of 75 patients with coronary artery disease (CAD) documented by greater than or equal to 50% diameter stenosis in 1 or more arteries and a control group of 47 subjects, 15 of them young volunteers and 32 with no or minimal coronary atherosclerosis and normal left ventricular function. All subjects underwent a symptom limited EST, with use of the Ellestad protocol. Signal-averaged P waves recorded before exercise, and for the first 6 minutes in recovery were measured using a 5x magnifier. The mean P duration before exercise in the control group was 107 +/- 16 ms (+/- 1 standard deviation) and 111 +/- 15 ms at the third minute of recovery, (p less than 0.001). In patients with CAD it was 112 +/- 12 and 129 +/- 19 ms (+/- 1 standard deviation), p less than 0.001, respectively. Differences in P-wave duration were found to be statistically significant (p less than 0.001) throughout recovery in the group with CAD when compared with control and maximal values at the third minute. The increase in P-wave duration (greater than or equal to 20 ms) was used as an additional parameter to exercise-induced ST-segment depression, ST elevation, or anginal pain for the test interpretation. The sensitivity increased from 57 to 75% and the specificity decreased from 85 to 77%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Significance of signal-averaged P-wave changes during exercise in patients with coronary artery disease and correlation with angiographic findings. 174 63


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