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)

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

Persons aged 85 years or more (n = 674) living in Tampere, Finland, were surveyed in 1977 and 1978. Five hundred fifty-nine persons (83%) were examined. Electrocardiographic findings, classified according to the Minnesota code, were compared with reported cardiac symptoms, clinical congestive heart failure, clinical coronary heart disease and relative cardiac volume on chest radiograph. Electrocardiographic items had a poor association with cardiac symptoms. ST-segment depression, T-wave inversion, ventricular premature complexes and atrial fibrillation were related statistically highly significantly to clinical congestive heart failure, as were ST-segment depression and T-wave inversion to clinical coronary heart disease. High left R waves, ventricular premature complexes and atrial fibrillation showed a significant association with cardiac enlargement (over 500 ml/m2) and pulmonary congestion in chest radiographs.
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PMID:Electrocardiogram, clinical findings and chest x-ray in persons aged 85 years or older. 315 9

The slopes of end-systolic pressure/end-systolic dimension and volume relations have been found to be relatively load-independent indices of left ventricular contractility. Noninvasive determination of these relationships has been performed in normal subjects and has been found to reflect baseline and drug-induced changes in ventricular contractility. Three late systolic indices of ventricular contractility were noninvasively determined in subjects with chronic congestive heart failure to determine the feasibility of the method and to assess the linearity and slopes of the relationships in this population. All relations were linear with individual correlation coefficients ranging from 0.86 to 0.99. The mean +/- SD slope was 42.8 +/- 26.4 mm Hg/cm for the end-systolic pressure-dimension relation, 0.59 +/- .42 mm Hg/ml for the end-systolic pressure-volume relation, and 48.7 +/- 32.2 mm Hg/cm for the peak systolic pressure-end-systolic dimension relation. All slopes were markedly reduced compared to those reported in normal individuals. The relative degree of depression was greater for the pressure-volume slope than for the pressure-dimension slope, which is explained by the relationship between volume and dimension in dilated ventricles. These data indicate that measurement of late systolic indices of ventricular contractility by this noninvasive technique is feasible in subjects with congestive heart failure and yields reduced slopes consistent with the diminished contractile state of this population. Pressure-volume rather than pressure-dimension relations may more accurately reflect inotropic state in dilated ventricles.
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PMID:Late systolic indices of ventricular function: noninvasive derivation in congestive heart failure. 318 44

To determine the prognostic implications of an early peak in plasma MB creatine kinase (MB CK) in patients with acute myocardial infarction who were not treated with an acute intervention, 342 patients with myocardial infarction confirmed by MB CK were retrospectively studied. The patients were classified into those with an early peak MB CK (less than or equal to 15 hours after the onset of symptoms, n = 84) and those with a late peak MB CK (greater than 15 hours after the onset of symptoms, n = 258). Patients with an early peak MB CK were slightly older, were more frequently female and had a higher incidence of prior myocardial infarction, congestive heart failure and arrhythmias compared with patients with a late peak MB CK. Patients with an early peak MB CK more frequently presented with ST segment depression (23 versus 11%, p less than 0.01), with anterior location of ischemia or infarction (71 versus 52%, p less than 0.01) and with a lower mean left ventricular ejection fraction (41.4 versus 47.4%, p less than 0.01). Despite more extensive left ventricular dysfunction at initial presentation, patients with an early peak MB CK had a smaller mean MB CK infarct size index (12.6 versus 18.9 g-Eq/m2, p less than 0.01), with no difference in the incidence of in-hospital complications, including death. The early left ventricular dysfunction improved in the patients with an early peak MB CK, evidenced by a 4.5% increase in ejection fraction from admission to 10 days after infarction, whereas the ejection fraction did not improve in patients with a late peak MB CK. However, the patients with an early peaking MB CK had myocardium in jeopardy as reflected by a higher incidence of ST segment depression and a decrement in the global left ventricular ejection fraction with exercise. The 4 year life table estimate for the rate of recurrent myocardial infarction after hospital discharge was higher in patients with an early peak MB CK (33 versus 22%, p less than 0.05), with an even more striking difference in the 4 year estimate for the rate of fatal recurrent infarction (20 versus 8%, p less than 0.001). The 4 year mortality estimate was markedly higher in hospital survivors with an early peak MB CK than in those with a late peak (47 versus 19%, p less than 0.0001) and, even after adjustment for differences in baseline characteristics, the residual excess mortality in those with an early peak was still significant (p less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Prognostic implications of an early peak in plasma MB creatine kinase in patients with acute myocardial infarction. 331 68

Changes in the pharmacokinetics of antiarrhythmic agents may be anticipated in patients with congestive heart failure (CHF), although the magnitude or direction of change is not always predictable. Factors complicating antiarrhythmic therapy in patients with CHF include both physiologic changes resulting from the disease state and unwanted effects of drug therapy for CHF. The volume of distribution is often significantly decreased (by as much as 50%) and loading doses should be reduced proportionately. Decreased blood flow to the liver and kidneys and decreased hepatic drug-metabolizing activity serve to diminish drug clearance. In some cases, simultaneous decreases in volume of distribution and clearance may result in little, if any, change in elimination half-life, despite higher plasma concentrations. Conversely, the elimination half-life of antiarrhythmic agents may be doubled in patients with CHF, necessitating a reduction in dosage. In the latter case, the time needed to reach steady state is lengthened, so that premature escalation of dosage may lead to excessive drug accumulation. In terms of their pharmacodynamics, most antiarrhythmic agents have a degree of negative inotropic effect at some concentration, and patients with reduced myocardial reserve are especially vulnerable to these effects. Some of the newer agents (such as tocainide, mexiletine, and encainide) appear to cause only minimal myocardial depression. Potential complications during therapy with all antiarrhythmic agents that are of special concern in patients with CHF include diuretic-induced hypokalemia, proarrhythmia, and possible interactions with cardiac glycosides and other drugs. Therapy for patients with CHF should be initiated with low doses of the agent selected, and the dosage carefully titrated while the patient is monitored, to confirm both efficacy and the absence of adverse effects. During subsequent outpatient therapy the patient should be carefully observed for sign of unexpected reactions, toxicity, or electrolyte imbalance.
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PMID:Pharmacokinetics and pharmacodynamics of antiarrhythmic agents in patients with congestive heart failure. 331 44

The newer dihydropyridine calcium antagonists are structurally related to nifedipine, but may provide greater vascular selectivity and wider clinical utility. Five new dihydropyridines-nisoldipine, nicardipine, nimodipine, felodipine and nitrendipine-are reviewed with regard to their preclinical pharmacology, haemodynamic effects and clinical indications. Nisoldipine is a potent arterial vasodilator with minimal electrophysiological and negative inotropic effects. Although data are still preliminary, the drug has shown some efficacy in both exertional angina and essential hypertension. The dosing interval is not yet clearly established, but may be twice daily. Utility in congestive heart failure awaits confirmation, but preliminary studies are promising. Nicardipine is an especially potent peripheral, cerebral and coronary arterial vasodilator that causes 10-fold less myocardial depression in animals than nifedipine, and may provide important cardioprotective effects during ischaemia. Human haemodynamic studies have confirmed nicardipine's lack of negative inotropism, its ability to reduce coronary and peripheral vascular resistance, and its lack of effect on cardiac conduction. Several controlled trials have documented its efficacy in exertional angina, vasospastic angina, and essential hypertension. Nicardipine's potential as an antiatherosclerotic agent is currently under investigation. Nimodipine is undergoing a unique clinical development programme aimed at cerebrovascular disorders. In almost all species, nimodipine selectively increases cerebral blood flow and reverses cerebral artery spasm without altering cerebral oxidative metabolism or systemic blood pressure. In humans, a large, double-blind, placebo-controlled trial in subarachnoid haemorrhage showed that nimodipine significantly reduced the severity of neurological deficits associated with delayed cerebral vasospasm. Several uncontrolled trials with larger numbers of patients support these results. Nimodipine has also proved useful in reducing cerebral artery spasm during intracranial surgery, and in the prophylactic treatment of migraine headaches. A preliminary study of nimodipine in acute stroke showed promising results in limiting neurological disability. Felodipine is a very potent systemic arterial vasodilator with negligible myocardial depressant activity. It is also a renal artery vasodilator. Unlike the other new dihydropyridines, felodipine prolongs the A-H interval on electrophysiological testing, but only to about 50% of that observed with verapamil. Felodipine is undergoing clinical trials in essential hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:'Second generation' dihydropyridine calcium antagonists. Greater vascular selectivity and some unique applications. 331 91

Studies of myocardial function in patients with hypophosphatemia have yielded conflicting results. Systolic time intervals were performed in 19 patients during and after the correction of hypophosphatemia; 11 had severe (0.9 +/- 0.15 mg/dL) and eight had moderate (1.4 +/- 0.11 mg/dL) hypophosphatemia. Controls were 14 patients with normal serum phosphorus levels. No patient with hypophosphatemia had clinical congestive heart failure. When hypophosphatemia was corrected, improvement in left ventricular performance was seen only in patients with severe hypophosphatemia (p less than 0.001); in eight patients left ventricular performance was normal during hypophosphatemia but showed significant improvement with its correction (p less than 0.01). Patients with moderate hypophosphatemia showed no significant change. Our results confirm the findings of O'Conner et al, whose study is the only previous one to demonstrate hypophosphatemia-induced myocardial depression in humans. Contradictory results from other studies may be explained by the inclusion of patients with moderate hypophosphatemia and failure to repeat measurements after the correction of hypophosphatemia. We conclude that reversible depression of myocardial performance is seen in hypophosphatemia only when it is severe. In some cases, normal left ventricular performance improves when hypophosphatemia is corrected.
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PMID:Reversible depression of myocardial performance in hypophosphatemia. 335 91

The authors present a case of a 62-year-old woman who was hospitalized with severe medical problems that included congestive heart failure secondary to mitral stenosis and atrial fibrillation, coronary artery disease, chronic renal failure, and a recent history of a right cerebral lacunar infarction. She also had a 2-year history of anxiety and depression, manifested in the hospital by frequent crying spells, sleeplessness, and ruminating about her illnesses. The patient received buspirone 5 mg three times a day for her anxiety and depression. Approximately 12 hours after her first dose, she developed dramatic myoclonus, dystonias, and akathisia. She was given 25 mg of intramuscular diphenhydramine and 1 mg of intramuscular benztropine mesylate, which resulted in little relief; however, 1 mg clonazepam caused both the myoclonic jerks and dystonias to resolve completely.
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PMID:Acute generalized myoclonus following buspirone administration. 337 31

Acromegaly involves cardiovascular complications mostly due to the presence of hypertension, diabetes and atherosclerosis. However the appearance of cardiac decompensation and arrhythmias in the absence of predisposing factors tends to support the hypothesis of a specific myocardiopathy caused by excess GH. In order to assess the existence and course of subclinical cardiac alterations, 8 acromegaly patients were examined: 4 males and 4 females aged 31-56 with GH levels of 24-70 ng/ml (M + CD X 47 +/- 16) and no cardiovascular symptoms. One of the patients had moderate hypertension and 2 reduced glucose tolerance. The basal ECG showed sporadic ventricular extrasystoles in 2 cases and alterations compatible with left ventricular hypertrophy in another, while the effort ECG produced an asymptomatic depression of the ST segment in the hypertensive patient. The chest X-ray was normal in all cases. The echocardiography study investigated: the thickness of the interventricular septum (IVS = 13.9 +/- 2.8 mm), the thickness of the posterior wall of the left ventricle (LPW = 10.6 +/- 2.9 mm), the septum/posterior wall ratio (IVS/LPW = 1.3 +/- 0.2 the diastolic diameter (DD = 15.4 +/- 11.4 mm), the fraction of shortening (FS = 39.1 +/- 14.5%), the ejection fraction (EF = 64.1 +/- 18.4%) and revealed asymmetrical septal hypertrophy in 3 cases, concentric hypertrophy in another two. In two cases the DD and EF were distinctly altered. The patients were re-examined 2-4 years after surgical or radiation treatment. GH levels (M +/- SD = 10.3 +/- 10.1 ng/ml) were normal in 4 cases and still high, though lower in another two. The remaining two patients had borderline GH levels with high Sm-C. The ECG and chest X-ray were unchanged while echocardiography revealed a significant deterioration in heart function as far as DD (56.4 +/- 10.8 mm, p less than 0.05) were concerned with frankly pathological results in 4 and 3 cases respectively. These data confirm the view that most acromegalic patients present subclinical abnormalities in cardiac function and that the evolution of these is slightly influenced by the reduction in GH and Sm-C. levels. In fact, while the persistence of high GH and Sm-C. levels may explain the progression of cardiac alterations in some cases, it does not in others. It is also emphasised that echocardiography appears to be the most sensitive non-invasive technique for the diagnosis and follow-up of cardiac involvement in acromegaly.
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PMID:[Cardiological findings in acromegaly]. 343 27

A prospective prognostic study of all admissions to a geriatric assessment and rehabilitation unit was carried out which analysed the medical profiles of 205 patients admitted for the first time during a four month period. All patients were followed up for at least six months after discharge. Particularly poor prognosis was noted among patients with renal failure, ischaemic heart disease, depression, pneumonia, congestive cardiac failure, trauma, mental disorder and dementia. Good prognosis was reported in patients with Parkinson's disease, faecal impaction, stroke and adverse drug reactions. Multiple diagnoses were common, and only nine patients had no active medical problems during their admission. The implications for adequate training of geriatricians in medicine are discussed.
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PMID:Medical profiles of patients admitted to a geriatric assessment and rehabilitation unit. 345 Nov 40


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