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)

Sotalol is a unique beta-blocker that prolongs repolarization. Its use in 626 patients with complex ventricular ectopic activity, as reported in the literature, resulted in suppression of arrhythmia in 50 to 60% of treatment attempts. Detailed analysis of data on arrhythmias in 356 patients that were entered prospectively into a database revealed a median reduction in ventricular premature beats of 76%, compared to a median suppression of repetitive ventricular ectopic activity of 91% and of episodes of nonsustained ventricular tachycardia of 97% (p = 0.002 vs reduction of ventricular premature beats). This marked antiarrhythmic potency of sotalol in repetitive ventricular arrhythmias is thought to be due to its class III activity. Drug efficacy was independent of age, sex, the presence or absence of organic heart disease and the degree of sotalol-induced prolongation of corrected QT interval. Evaluation of left ventricular function in 215 patients treated with the drug demonstrated that depression of left ventricular ejection fraction occurred far less frequently than expected with conventional beta-blockers. Even patients with severely depressed pump function tolerated sotalol surprisingly well. There is a propensity of the drug to aggravate arrhythmia, which resulted in serious proarrhythmic events in 30 (3.5%) of 853 patients. These often consisted of torsades de pointes (9 of 30 patients). Proarrhythmia occurred primarily within the first 3 days of dosing, and exhibited a dose-dependence. In conclusion, sotalol is an effective and well-tolerated antiarrhythmic drug in patients with complex ventricular ectopic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
Int J Cardiol 1992 Dec
PMID:Efficacy and safety of sotalol in patients with complex ventricular arrhythmias. 128 7

The clinical implications of isolated late recovery ST depression were tested in patients with scintigraphically defined ischemia (coronary artery disease [CAD], n = 18) compared with patients without ischemia (n = 25). Spontaneous (78.4 versus 12.0%, P < 0.008) and exercise-induced angina (44.4 versus 0%, P < 0.0001) were more frequently seen in patients with CAD. Histories of unstable angina (33.3%), prior myocardial infarction (27.8%), ST elevated angina (22.2%) and significant stenosis in the left anterior descending artery (17 of 18, 94.4%) were almost exclusively seen in the CAD group. There was no significant difference between the two groups in capacity for exercise, maximum deviation of ST level or TV2 amplitude. Balloon angioplasty abolished late recovery ST changes in 63.6% of CAD patients. These results suggest that isolated late recovery ST depression, when accompanied with typical chest pain, may be considered as an indicator of myocardial ischemia, but this phenomenon is difficult to distinguish electrocardiographically.
Can J Cardiol 1992 Dec
PMID:Isolated post exercise delayed ST depression as a sign of severe ischemia: the influence of percutaneous transluminal coronary angioplasty. 128 36

Disopyramide is a Vaughan-Williams class Ia antiarrhythmic, which is distinguished by its anticholinergic activity, which is due to its active metabolite: mono-N-alkyl disopyramide. In cells with a rapid response, such as those in the His-Purkinje tissue, it depresses conduction. In slow-responding cells (sinus node and Tawara's node) direct depression of conduction and automatism, and anticholinergic stimulation have opposing effects. In terms of clinical electrophysiology, this is a Touboul class IIa compound: and action mainly on the His-Purkinje system involving extension of the conduction time and of the refractory time. Nodal conduction is improved according to measurement of the alternate Wenckebach; according to studies of the denervated heart in transplanted patients, there is a depressant effect on automatism and conduction at all levels, but the vagolytic effect corrects this activity at Tawara's node. Clinical trials have demonstrated the absence of any deterioration, and in some cases and actual improvement of nodal conduction disorders in response to disopyramide and good safety in the presence of non-major intraventricular conduction problems (such as bundle branch block). In practice, these properties mean that moderate nodal conductive disorders and simple bundle branch block do not constitute an obstacle to the use of disopyramide. In junctional tachycardia, it is particularly indicated for use in tachycardia involving an accessory pathway, but is also effective in intranodal tachycardia due to its twofold action.
Ann Cardiol Angeiol (Paris) 1992 Oct
PMID:[Effects of disopyramide on normal and pathological atrioventricular conduction]. 129 85

The respiratory effects of pymadin, amiridine, thyrotropin-releasing hormone (TRH), its analog RGH 2202, and pentetrazol and their interaction with morphine were studied in anesthesized rats. During intravenous injection or local application to the medulla oblongata, pymadin, amiridine, TRH and RGH 2202 were shown to enhance the respiratory activity of the diaphragm and to abolish its morphine-induced inhibition. TRH and RGH 2202 proved to be the most potent and safe antagonists of morphine-induced respiratory depression. These agents given in the doses sufficient to completely abolish morphine-induced respiratory depression unchanged its antinociceptive activity. Pentetrazol in the tested dose range failed to increase diaphragmatic respiratory activity or to eliminate its depression induced by morphine.
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PMID:[Central nervous system stimulants as nonspecific antagonists of morphine-induced respiratory depression]. 130 43

Cardiac hypertrophy is an adaptive response to an increased load imposed on the myocyte which allows the heart to perform increased work while maintaining normal myocardial fiber stress and shortening in systole. A deleterious consequence of pressure-overload hypertrophy is the prolongation of Ca(2+)-sensitive force inactivation (impaired myocardial relaxation) which is related to intrinsic alterations in cytosolic Ca2+ transport and reuptake in diastole. Additional factors appear to adversely modify myocardial relaxation in the hypertrophied heart, including the imposition of ischemia. There is also evidence that the expression and activity of the cardiac tissue renin angiotensin system (RAS) may be modified in the hypertrophied heart and contribute to diastolic dysfunction. Recent studies have demonstrated the presence of increased cardiac angiotensin converting enzyme (ACE) mRNA expression and activity in animal models of hypertrophy, including the aortic-banded rat with compensatory pressure-overload hypertrophy and rats with post-infarction remodeling. In the beating, isovolumic aortic-banded rat heart, the increased intracardiac activation of angiotensin I to II has been shown to be associated with a dose-dependent depression of diastolic relaxation. Preliminary studies suggest that the depression of diastolic function by angiotensin II in the hypertrophied heart can be prevented by the specific inhibition of cardiac ACE. In addition, the well-recognized susceptibility of the hypertrophied heart to severe ischemic diastolic dysfunction also appears to be favorably modified by the inhibition of cardiac ACE activity. The mechanisms responsible for the adverse effects of angiotensin II on diastolic relaxation in the hypertrophied heart are likely to be complex.(ABSTRACT TRUNCATED AT 250 WORDS)
Basic Res Cardiol 1992
PMID:Diastolic dysfunction in pressure-overload hypertrophy and its modification by angiotensin II: current concepts. 133 63

Myothermal measurements of tension-independent heat are used to calculate the quantity of calcium released during isometric contraction and the rate at which it is removed in control, thyrotoxic and pressure-overloaded rabbit hearts. Experiments were carried out at 30 degrees C. In control rabbit hearts 41.0 +/- 7.0 nmoles/g Ca++ was released into the cytosol for each beat, while the rate at which the Ca++ was removed from the cytosol was 24.4 +/- 4.4 nmoles/g sec. In the presence-overloaded preparations, the amount of calcium released and the rate of calcium removal were 41% and 40% of control values. This reduction was correlated with the mRNA levels for the sarcoplasmic reticulum (SR) Ca++ ATPase, phospholamban and the ryanodine receptor. The depression was also correlated with a reduction in SR Ca++ ATPase protein expression. In thyrotoxic hearts compared with controls, with each activation there is an increase in the amount of calcium liberated into the cytosol (39%) and the rate of calcium removal (31%). This increase is correlated with an increase in the mRNA and protein expression for the SR Ca++ ATPase as well as the mRNA for the ryanodine receptor. Calsequestrin mRNA was unchanged in all of the experimental preparations. It is suggested that the alteration in the calcium cycling proteins offers at least a partial explanation for the changes in calcium cycling measured in response to the stresses applied.(ABSTRACT TRUNCATED AT 250 WORDS)
Basic Res Cardiol 1992
PMID:The regulation of calcium cycling in stressed hearts. 133 66

To evaluate the prognostic and clinical significance of silent myocardial ischemia (SMI), we examined cardiac events in 160 patients with old myocardial infarction who underwent ambulatory Holter monitoring, treadmill exercise testing and coronary angiography. Using the Cox's proportional hazard regression model and the survival curves with the Kaplan-Meier method, we identified the predictors of cardiac events. The incidence of cardiac events for all the patients during the 44-month follow-up period was 18%. The significant predictors of unfavorable outcomes were severe coronary lesions and SMI. The incidence of SMI was 38%. The cardiac event rate in patients with SMI was higher than in those without SMI (32 vs 9%, p < 0.05). The most frequent cardiac event in patients with SMI was reinfarction, and the significant predictors of cardiac events for these SMI patients were lower ejection fraction and maximum ST depression on Holter monitoring. In conclusion, SMI proved to be a significant predictor of unfavorable outcome in patients with old myocardial infarction. It was, therefore, suggested that revascularization (PTCA/CABG) should be used as early as possible in patients with SMI whether anginal symptoms are present or not.
J Cardiol 1992
PMID:[Silent myocardial ischemia in myocardial infarction patients: its prognostic significance]. 133 98

The anaerobic threshold (AT) is regarded an objective parameter for evaluating exercise tolerance, but its relationship to the improvement of myocardial ischemia remains uncertain. To investigate this relationship, submaximal treadmill exercise tests were performed for 15 consecutive patients with angina pectoris who had undergone successful percutaneous transluminal coronary angioplasty (PTCA). Before and after PTCA, the AT was determined using cardiorespiratory monitoring, while the patients were receiving their usual vasodilator medications. 1) Before PTCA, the minute oxygen uptake (VO2) at the AT correlated well with the peak VO2 (r = 0.92, p < 0.002). The VO2 at the AT, however, showed less correlation (r = 0.71, p < 0.002) with the VO2 at ST segment depression, while the latter parameter correlated closely with the peak VO2 (r = 0.91, p < 0.002). 2) After PTCA, exercise time, peak VO2, and the double product at peak exercise increased significantly (from 640.1 +/- 212.2 to 772.9 +/- 230.0 sec, p < 0.001, from 19.1 +/- 5.2 to 22.4 +/- 4.9 ml/min/kg, p < 0.05, and from 19.7 +/- 5.0 x 10(3) to 23.7 +/- 4.5 x 10(3), p < 0.001, respectively). However, the VO2 at the AT did not increase significantly (from 15.8 +/- 4.1 to 16.6 +/- 3.5 ml/min/kg, p = NS). The heart rate, systolic blood pressure, and double product at the AT did not change significantly. In conclusion, in patients with angina pectoris, the AT is apparently related to the onset of myocardial ischemia. However, the AT does not necessarily reflect acute improvement of myocardial ischemia immediately after PTCA.
J Cardiol 1992
PMID:The effect of percutaneous transluminal coronary angioplasty on anaerobic threshold in patients with angina pectoris. 134 27

At the cellular and molecular level the transition to heart failure is a complex process that involves structural adaptation, not only of the heart, but of peripheral vasculature and renal tissues as well. Recent studies have suggested that autocrine, paracrine, and circulating biologically active mediators activate events that result in the concerted failure of adaptive mechanisms and the ultimate depression of cardiac myocyte function. Greater understanding of these local mechanisms in the future may lead to drug therapies that can selectively block these mechanisms and prevent the progression from compensation to overt heart failure.
Am J Cardiol 1992 Oct 08
PMID:Autocrine and paracrine mechanisms in the pathophysiology of heart failure. 135 50

The effects of 5 and 10 mg of amlodipine and of placebo were compared in 21 patients with stable angina pectoris and multivessel coronary artery disease. The blind comparison was performed by means of bicycle ergometry and stress echocardiography using esophageal stimulation of the left heart atrium. All patients subsequently received placebo, amlodipine 5 mg and 10 mg for 2 weeks. In bicycle ergometry both doses of amlodipine in comparison with placebo significantly lowered the ST segment depression in lead V5 and prolonged the time to onset of angina. The exercise duration was significantly prolonged only after 10 mg of amlodipine. In stress echocardiography 10 mg of amlodipine significantly improved ejection fraction and reduced wall motion score during stimulation and increased peak velocity of relaxation of left ventricular posterior wall at rest and immediately after stimulation. In the patients with left ventricular end-diastolic pressure < or = 20 mmHg, amlodipine reduced the ratio of peak transmitral flow velocity in atrial contraction to that in early diastole (A/E) at rest and shortened deceleration time at rest and immediately after stimulation. Amlodipine in patients with stable angina pectoris significantly improved the exercise tolerance and the function of the left ventricle in a dose-dependent way. Amlodipine was well tolerated.
Int J Cardiol 1992 Oct
PMID:Amlodipine in patients with stable angina pectoris treated with nitrates and beta-blockers. The influence on exercise tolerance, systolic and diastolic functions of the left ventricle. 135 30


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