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)

One-year follow-up data on 515 patients who survived hospitalization with MB-creatine kinase-confirmed, acute non-Q wave myocardial infarction were analyzed for factors related to mortality (n = 57) and late reinfarction (n = 64). Twelve of 24 analyzed variables were significantly associated with mortality. Those factors, which were independently predictive of mortality by Cox regression analysis, were persistent ST depression (p = 0.0009), a history of congestive heart failure (CHF) (p = 0.0069), older age (p = 0.0128), and ST elevation at hospital discharge (p = 0.0173). In-hospital reinfarction achieved borderline significance (p = 0.0512). Mortality during the follow-up period was 5.5% in patients with no ST depression, 10.1% in those with ST depression at baseline or discharge, and 22.2% in patients with ST depression at baseline and discharge (i.e., "persistent" ST depression). The age-adjusted risk of mortality for patients with persistent ST depression, discharge-ST elevation, and CHF was 13.99 times as high as was the risk for patients with no ST depression, no discharge-ST elevation, and no CHF. Of the 483 patients with complete electrocardiographic data at both baseline and discharge, 203 (42%) could be stratified into a high risk population with a risk ratio for 1-year mortality more than sevenfold that of patients with no risk factors. Although persistent ST depression was significantly associated with several measures of structural left ventricular damage, the independent significance of ST depression persisted even after adjusting for these factors. The independent predictors of late reinfarction (persistent ST depression, p = 0.0058; Killip class II or III, p = 0.0106; and left ventricular hypertrophy, p = 0.0470) permitted a similar risk stratification. We conclude that 1) easily identified clinical and electrocardiographic factors permit stratification of patients with non-Q wave infarction into high-risk subsets who may benefit from aggressive therapy; 2) ST depression is a highly significant and independent predictor of poor prognosis; and 3) the powerful predictive value of persistent ST depression suggests that non-Q wave myocardial infarction patients with this depression should be viewed as potentially high-risk patients who may be candidates for additional noninvasive testing or early coronary angiography.
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PMID:Risk stratification of patients with non-Q wave myocardial infarction. The critical role of ST segment depression. The Diltiazem Reinfarction Study Research Group. 280 57

The value of atrial pacing and thallium-201 scintigraphy for assessing risk of subsequent cardiac events was examined in 210 patients with stable chest pain. Follow-up information was complete in 195 patients (mean age 61 years). Over an average follow-up of 19 months, cardiac events occurred in 38 patients--unstable angina in 20, nonfatal acute myocardial infarction in 6 and death from cardiac causes in 12. A history of previous myocardial infarction, diabetes mellitus, systemic hypertension or peripheral vascular disease at the time of pacing was not associated with an increased frequency of subsequent cardiac events. Six of 38 patients with later cardiac events had a history of congestive heart failure, compared with 8 of 157 without cardiac events (p less than 0.05). Neither pacing-induced angina, ST depression, nor the presence of a fixed perfusion defect was significantly more frequent in patients with cardiac events as a whole compared with patients without such events. Reversible defects and abnormal scans (reversible or fixed defects) were present, respectively, in 19 and 31 of 38 patients with cardiac events, compared with 42 and 79 patients, respectively, of the 157 patients without cardiac events (both p less than 0.01). In patients who developed unstable angina, a reversible defect was seen in 13 and an abnormal scan in 16 (both p less than 0.01 compared with patients without cardiac events). In 12 patients who died from a primary cardiac event, fixed defects were present in 8 and an abnormal scan in 11 (p less than 0.05 and p less than 0.01, respectively, compared with patients without cardiac events).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prognostic value of atrial pacing and thallium-201 scintigraphy in patients with stable chest pain. 281 58

1. LND 623 and LND 796 are two aminosteroid derivatives which exert similar positive inotropic effects to digitalis. Their electrophysiological, toxic and inotropic effects were investigated in both normal and partially K+-depolarized ventricular muscle. 2. In guinea-pig myocardial fibres, LND 623 and LND 796 required tenfold higher concentrations than digoxin to induce the same signs of toxicity; e.g. triggered activities generated from delayed afterdepolarizations, leading to the marked depression of action potential characteristics and inexcitability. These abnormal rhythms and delayed afterdepolarizations were abolished by 1 mM caffeine. The toxic effects were reversed by washout, particularly in the case of LND 796. 3. In normal-K+ solution, LND 623 and LND 796 exhibited concentration-dependent positive inotropic effects on guinea-pig papillary muscle and increased concomitantly resting membrane potential and action potential amplitude. The range of active concentrations (0.1 to 1 microM) of LND 623 was larger than that of digoxin (0.3 to 1 microM). Like digoxin, LND 796 exerted negative inotropic effects at the lowest concentrations (0.01 to 0.03 microM) and positive inotropic effects at high concentrations (1 and 3 microM). 4. In partially K+-depolarized papillary muscle, in the presence of 2 microM histamine, LND 623 (3 and 10 microM) and LND 796 (10 and 30 microM) enhanced the two components P1 and P2 of the contraction and increased slow action potential amplitude, resting potential and maximal rate of depolarization. Low concentrations (0.03 to 0.3 microM) of LND 796 induced negative inotropic effects. beta-Adrenoceptor blockade with atenolol (1 microM) did not modify the activity of LND 623 but significantly enhanced the negative inotropic effect on P2 induced by 1 and 3 microM LND 796 and reduced the positive inotropic effect on P1 and P2 of the highest concentration (30 microM) studied. 5. In the presence of either caffeine (1 mM) or Ca2+-free, Sr2+-rich (3.6 mM) solution, LND 623 and LND 796 produced a positive inotropic effect which was stronger with LND 623. 6. It is suggested that two mechanisms are involved in the inotropic effects of these aminosteroids: (i) an enhanced Ca2 + entry via the slow calcium channels partially brought about by a local release of endogenous catecholamines in the case of LND 796, (ii) an inhibitory effect on Na+-K+ ATPase which, at the highest concentrations, lead to similar signs of cellular toxicity to those described for digitalis drugs. Because of their enlarged positive inotropic range, both aminosteroids may be of interest in the treatment of congestive heart failure.
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PMID:Electrical and mechanical effects of new aminosteroids on guinea-pig isolated ventricular muscle. 285 56

The effects of acute intravenous administration of ICI 118,587 (Corwin), a partial beta 1 agonist, were studied in nine patients with dilated cardiomyopathy and symptomatic congestive heart failure. Hemodynamic and metabolic parameters were measured using Swan-Ganz, arterial, and coronary sinus catheters. Repeated doses of Corwin produced no significant change in left ventricular performance, while a trend towards decreased blood pressure and stroke work was seen. No change occurred in coronary sinus blood flow, transmyocardial lactate extraction, or catecholamine release. One patient had significant depression of left ventricular function with hypotension. Thus, acute infusion of Corwin produced no beneficial inotropic responses, but rather produced features suggestive of further myocardial depression.
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PMID:Acute hemodynamic and metabolic effects of ICI 118,587 (Corwin), a selective partial beta 1 agonist, in patients with dilated cardiomyopathy. 286 73

The value of beta blockade after myocardial infarction is extremely well documented. Close to 50 randomized trials have been performed, involving about 40,000 patients with short- or long-term follow-up. Over 20,000 patients have been included in more than 20 placebo-controlled trials with a follow-up period of 3 months or more. In long-term follow-up studies, about 1 to 2 weeks to 1 year after myocardial infarction, mortality was reduced by 21% and reinfarction by 24% (about 20,000 patients in 24 trials). The trial medication was withdrawn in about 20% in both placebo and beta-blocker groups in the major trials. In addition to reduction of mortality and reinfarction rate, benefits have clearly been demonstrated on severity of chest pain, arrhythmias, and other thromboatherosclerotic complications, as well as on readmissions. Significantly more patients experienced congestive heart failure, hypotension, bradycardia, and cold hands with beta-blocker treatment, whereas no clear-cut difference was found for atrioventricular block, bronchial constriction, and intermittent claudication. Some studies have reported more tiredness, depression, and gastrointestinal disturbances. In the Stockholm metoprolol trial, analyses on quality of life have been performed. In this trial, 3 years of metoprolol treatment after myocardial infarction resulted in a prolongation of both survival and time spent completely asymptomatic, as well as in an optimal functional state. Furthermore, less time was spent disabled after serious atherosclerotic complications. Long-term beta blockade after myocardial infarction reduces mortality and morbidity but causes adverse reactions in some patients. With proper selection of patients and type and dosage of beta blocker, survival without atherosclerotic complications and side effects can be prolonged.
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PMID:Use of beta blockers in postinfarct prophylaxis: aspects on quality of life. 288 38

Oral angiotensin converting enzyme inhibition was introduced eight years ago and is becoming increasingly popular for the treatment of hypertension and congestive heart failure. This treatment causes blood pressure lowering associated with suppression of angiotensin and aldosterone, lack of orthostatic hypotension or metabolic disturbances, redistribution of regional blood flows in favor of vital organs and, in the long term, decreased sympathetic drive and regression of left ventricular hypertrophy. It is effective as monotherapy in more than 50 percent of unselected patients; addition of a diuretic increases the percentage of responders to more than 80 percent. It is the treatment of choice for patients with concurrent diabetes, asthma, gout, depression, or very active life-style. Side effects, observed originally in patients with severe hypertension and renal failure treated with very high doses of captopril, are rare in otherwise healthy hypertensive patients receiving smaller doses of this drug and virtually absent with second-generation angiotensin converting enzyme inhibitors like enalapril.
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PMID:Clinical utility of angiotensin converting enzyme inhibitors in hypertension. 302 82

Since their introduction in clinical practice in 1980, ACE inhibitors have been found useful in the treatment of hypertension and CHF. In hypertension, they are effective as monotherapy in 40% to 50% of the patients, and in combination with diuretics or calcium antagonists, they are effective in up to 85% of the patients. They are well tolerated, are not associated with depression, impotence, bronchospasm or metabolic derangements such as hypokalemia, hyperuricemia or hyperglycemia, and do not have adverse effects on the quality of life. As a result, they are preferred in hypertensive patients with CHF, left ventricular dysfunction, mental depression, older age, coronary artery disease, metabolic disorders, chronic destructive pulmonary disease, and peripheral vascular disease. In CHF they cause long-lasting hemodynamic and symptomatic improvement, improve exercise tolerance, and may lower mortality in certain patient subsets. Evolving new indications for ACE inhibitors include the diagnosis of renovascular hypertension, the prediction of surgical success, the treatment of scleroderma renal crisis, the reduction of proteinuria, renal protection, cardioprotection, the improvement of arterial compliance, in Bartter's syndrome and idiopathic edema, etc. ACE inhibitors are usually well tolerated but in some instances they may cause class-specific side effects such as hypotension; usually reversible azotemia or renal failure, especially in patients with renal artery stenosis or with CHF with low blood pressure; cough; angioedema; and hyperkalemia. Differences among ACE inhibitors are emerging and include chemical class (e.g., zinc ligand), biotransformation, potency, pharmacokinetics, prodrugs, tissue effects, additional pharmacologic properties, and drug interactions.
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PMID:Angiotensin converting enzyme inhibitors. II. Clinical use. 305 46

Changes in the pharmacokinetics of antiarrhythmic agents should be expected in patients with congestive heart failure (CHF). The direction of the changes, however, is not always predictable. The volume of distribution is often decreased by as much as 40%, and loading doses should, therefore, be appropriately reduced. Drug clearance may also be diminished due to decreased blood flow to the liver and kidneys, as well as decreased hepatic drug-metabolizing activity. Infusion rates should similarly be lowered to avoid toxicity. However, decreases in both volume of distribution and clearance may result in little, if any, change in elimination half-life, despite higher plasma concentrations. On the other hand, the elimination half-life of antiarrhythmic agents that have a large volume of distribution and are highly cleared by the liver may be twice as long in patients with CHF compared with normal subjects. Thus, the total daily dose of drug should also be lower in these patients. In addition, the time necessary to reach steady state is longer, so that premature dose escalation may lead to excessive drug accumulation. In terms of their pharmacodynamic effects, all antiarrhythmic agents have the potential to manifest a degree of negative inotropy, which must be anticipated as a possible side effect in patients with CHF. Some of the newer agents, such as tocainide and encainide, appear to cause only minimal myocardial depression. Other potential complications of all antiarrhythmic therapy include proarrhythmia and possible drug interactions with digitalis and diuretics.
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PMID:Effects of congestive heart failure on the pharmacokinetics and pharmacodynamics of antiarrhythmic agents. 308 Aug 60

The long-term efficacy of digoxin maintenance therapy must be determined individually for patients with normal sinus rhythm who have a history of congestive heart failure but no remaining signs or symptoms. Predictive factors for successful discontinuation of the agent in the elderly include normal mental status (including absence of depression), ability to adequately perform activities of daily living, general feelings of well-being, absence of multiple organic disease, absence of multiple drug use, and no evidence of existing congestive heart failure or atrial fibrillation. Our findings indicate that physicians and patients need to reexamine the concept that congestive heart failure is necessarily a chronic disease. Certainly, evidence exists that continuing digitalis therapy indefinitely is inappropriate and may be harmful. Further investigation may prove that congestive heart failure in the elderly, like pneumonia, is a common acute occurrence and in many cases not a chronic state for which patients are destined to receive medication indefinitely. We hope that the findings from our small sample will stimulate other investigators to question the indiscriminate long-term use of digitalis in the elderly.
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PMID:Digitalis for congestive heart disease in the elderly. A family practice view of the efficacy of long-term therapy. 310 Oct 52

The effects of intravenous acetylsalicylic acid (1.0 g bolus) on renal function and prostaglandin synthesis were evaluated in a prospective, controlled study in eight patients in an intensive care unit. Four of these patients had congestive heart failure. Administration of acetylsalicylic acid caused significant antidiuresis (-56%), antinatriuresis (-82%), renin suppression (-26%) and decreased GFR (-41%). All of these changes were completely reversible within 1-2 hours and tended to be more pronounced in the patients with congestive heart failure. Urinary excretion of prostaglandin E2 was depressed profoundly (-93%) and did not return to more than 45% of control 6 h after the administration of acetylsalicylic acid. We conclude that intravenous acetylsalicylic acid affects kidney function in a manner similar to other prostaglandin synthesis inhibitors. Its effects are, however, short-lived. The inhibition of urinary PGE2 excretion outlasts GFR depression, antidiuresis, antinatriuresis and renin suppression by several hours.
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PMID:Effects of intravenous aspirin on prostaglandin synthesis and kidney function in intensive care patients. 311 Jun 70


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