Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amiodarone, a commonly used antiarrhythmic agent, has numerous adverse effects. The purpose of this case report is to highlight its hepatotoxicity, an unusual complication of long term amiodarone therapy. Our patient is a 76-year-old man with underlying ischaemic heart disease and recurrent ventricular tachycardia. Eleven months after commencing amiodarone, he developed asymptomatic raised aminotransferases which resolved following drug withdrawal. Amiodarone was then reintroduced and four years later, the patient developed hepatomegaly, worsening liver biochemistry and histopathological changes consistent with early cirrhosis. His symptoms improved following discontinuation of amiodarone. However, hepatomegaly and a low serum albumin still persist four years later.
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PMID:Hepatotoxicity of amiodarone. 129 29

Deprenyl is a synthetic, selective inhibitor of the monoamine oxidase-B enzyme system. The mechanism of its beneficial effect in early and advanced Parkinson's disease is not settled. Increased striatal dopamine accumulation, sensitization of surviving dopamine neurons with increased dopamine production and reduced nigro-striatal toxicity may all contribute. The standard daily dose of deprenyl is 10 mg. Selectivity may be lost at higher doses. Deprenyl is especially indicated in untreated patients, improving up to 50 percent of patients with mild motor fluctuations. Major symptomatic benefit also occurs in occasional levodopa treated patients. Adverse effects are common, however. Increase dyskinesias, confusion and hallucinations, nausea and postural hypotension may necessitate drug withdrawal or the use of low dose regimens. Caution should be exercised with older patients, those with ulcer disease, which may be worsened by deprenyl, and individuals with active ischemic heart disease where the safety of this drug is not yet clear.
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PMID:Deprenyl in Parkinson's disease: mechanisms, neuroprotective effect, indications and adverse effects. 157 60

Patients with stable coronary artery disease commonly have transient myocardial ischemia with or without experiencing angina, but the prognostic implications of this "total ischemic burden" is still a matter of debate. We studied 112 consecutive patients with coronary artery disease, normal left ventricular function at rest and exercise-induced myocardial ischemia, a 24-hour ambulatory EKG was performed after drug withdrawal. The mean exercise duration was 572 +/- 192 seconds, with an ischemic threshold (ST depression = 1 mm) of 390 +/- 190 seconds). By Holter monitoring 30 patients had no ischemia and 82 (73%) had a total of 332 episodes of ST segment changes, the majority of which were asymptomatic (242/332, 73%). Among 82 patients with transient myocardial ischemia, 44 (54%) had only asymptomatic episodes. Nine patients (11%) complained of angina coincident to ST changes. Twenty-nine patients (35%) had both painful and painless ST segment alterations. All patients were prospectively followed-up while on conventional medical therapy. During a mean follow up of 25 +/- 10 months cardiac events occurred in 31 patients; there were 5 cardiac deaths, 3 non-fatal myocardial infarctions, 2 hospitalization for unstable angina and 21 revascularization procedures (PTCA or CABG). By multivariate analysis the number of stenotic vessels on coronary angiography was predictive of the events during the follow-up (p = 0.03), while other demographic, clinical, ergometric and angiographic variables were not influential. Event-free survival was similar for all subsets of transient myocardial ischemia (silent, symptomatic, or none).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prognostic value of total ischemic burden in patients with stable ischemic heart disease. 176 34

To assess acute hemodynamic effects and exercise capacity of an intravenously administered single dose of captopril and to compare the acute response with chronic variation in hemodynamic and functional parameters after long-term oral administration, (in order to determine the profile of responders and non-responders) we studied 12 patients with chronic congestive heart failure due to primary dilated cardiomyopathy (11 pts) and ischemic heart disease (1 pt). Hemodynamic response was assessed using transthoracic electric impedance with cardiac output measurement. The exercise capacity was determined using multistage bicycle ergometer symptoms limited stress test. The hemodynamic and functional evaluation--resting cardiac output, exercise capacity (Ex. Dur.) and cardiac output rise at maximum workload (% CO)--were investigated at first as a control; after i.v. captopril administered in 10 min (25 mg) (acute); after captopril per os (25-75 mg for 30 days) (chronic) and after 5 days of withdrawal (wash out). (Table: see text). Improvement of left ventricular performance mainly during exercise after acute and chronic administration of captopril occurred, as evidenced from cardiac output increase at maximum work load, and rise of exercise duration. Moreover, our data suggest that captopril may have a sustained beneficial effect, for a few days, even after drug withdrawal. Nevertheless, the lack of correlation in single cases between acute and chronic response, also indicates that captopril deserves further study to determine its role in acute and/or chronic management of congestive heart failure in order to choose the ideal strategy.
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PMID:[Acute and long-term effects of captopril in patients with left ventricular dysfunction and dilatation: evaluation of function and work capacity]. 269 86

Stress testing was carried out by two stressors, mental arithmetic and Sacks-Levy's test in randomized sequence, in 64 male patients with a mean age of 51 +/- 7 years in NYHA Classes I or II within 3 months after acute myocardial infarction. The stress profile was obtained after drug withdrawal by continuous recording of electrocardiogram, frontal electromyogram, and peripheral skin temperature and conductance. Blood pressure was measured each minute by cuff. The patients were subdivided into 4 groups of 16 each and were studied in an identical fashion after a 48-h oral treatment with propranolol 120 mg daily, atenolol 100 mg daily, chlordesmethyldiazepam 2 mg daily, or placebo. During stress, signs of myocardial ischemia or pump failure were not observed; minor arrhythmias were recorded. Cardiovascular activation was observed with significant increments (p less than 0.001) in heart rate, systolic and diastolic blood pressures in all 4 groups for both stressors with a slightly greater effect of mental arithmetic; Sacks' test was more effective on the frontal electromyograph response. Following beta blockade the stress profile of heart rate was significantly lower and flattened. The stress profile of blood pressure was also lower, but the reduction in the increment during stress was not significant. No differences were observed in the effects of the two beta blockers; no significant changes were evident in the stress profile of the noncardiovascular psychophysiologic indexes. Stress profiles were not altered by the benzodiazepine. In conclusion beta-blocker agents seem to be more useful than anxiolytic drugs in preventing cardiovascular activation induced by mental stress in patients with recent myocardial infarction.
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PMID:Effects of propranolol, atenolol, and chlordesmethyldiazepam on response to mental stress in patients with recent myocardial infarction. 288 16

Abrupt withdrawal of calcium channel blocking agents has been associated with symptoms of ischemic heart disease, but acute myocardial infarction has not been noted. Herein is described a severely uremic patient who had an acute myocardial infarction shortly after discontinuance of diltiazem, although results of subsequent coronary arteriography were normal. It is postulated that myocardial damage occurred because of increased intracellular calcium flux, augmented myocardial contractility, and/or drug withdrawal-related coronary spasm.
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PMID:Myocardial infarction with normal results of coronary angiography following diltiazem withdrawal. 372 13

To determine the hemodynamic and clinical effects of long-term positive inotropic stimulation on the myocardium, we treated 31 patients with severe chronic heart failure with oral amrinone (600 mg daily) and performed invasive hemodynamic studies during short- and long-term treatment with the drug. Stroke volume and stroke work indexes increased markedly during the first 48 hr of therapy (p less than .01) but returned to pretreatment values after 2 to 10 weeks; upon drug withdrawal, both variables deteriorated rapidly to values significantly lower than those observed before treatment with amrinone (p less than .01), despite similar values for left ventricular filling pressure, mean arterial pressure, and systemic vascular resistance. This pattern of response indicated that progression of the underlying heart disease had occurred during treatment with amrinone and contributed importantly to its failure to produce long-term benefits. Progression of left ventricular dysfunction was associated with a progressive increase in heart rate and plasma renin activity and a decline in serum sodium concentration. Clinically, amrinone therapy was complicated by sustained symptomatic ventricular tachycardia in four patients, worsening myocardial ischemia in four patients, and worsening congestive heart failure in eight patients, all of whom had been stable before entry into the study; only three of the 31 patients improved clinically. Ten patients died during the first 2 weeks of treatment, and 16 (52%) were dead within 3 months, a mortality rate twice as great as that seen during comparable trials with vasodilating drugs. Although noncardiac adverse effects were frequent, they were not the primary reason for drug failure. In conclusion, long-term therapy with amrinone may accelerate progression of left ventricular dysfunction, exacerbate myocardial ischemia, and provoke life-threatening ventricular tachyarrhythmias, thereby shortening survival in patients with severe chronic heart failure. Prolonged administration of inotropic drugs may achieve short-term gains at the expense of long-term detrimental effects on the myocardium.
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PMID:Hemodynamic and clinical limitations of long-term inotropic therapy with amrinone in patients with severe chronic heart failure. 638 99

The aims of this study were to determine: (1) the proportion of elderly hypertensive subjects currently attending a hospital hypertension clinic suitable for a trial of antihypertensive drug withdrawal, (2) the proportion of suitable patients who can be successfully withdrawn from drug therapy while receiving nonpharmacological advice, and (3) the factors associated with successful withdrawal. One hundred and five consecutive hypertensive subjects, 53% female, mean age 76 years (range 65-84 years) on pharmacological antihypertensive therapy for > 1 year were studied, of whom 78 (74%) had a clinic SBP < 175 mmHg and DBP < 100 mmHg. Subjects with recent myocardial infarction or stroke or with symptoms of ischaemic heart disease were excluded. Antihypertensive drug therapy was withdrawn in this group and nonpharmacological advice to lower BP was instituted. Clinic BP and weight were subsequently recorded monthly for 12 months in all subjects and at every three months in those who had a possible follow-up period of 24 months. The 24h ambulatory BP was measured at baseline and repeated one month off therapy; 24h urine electrolytes were also assessed at baseline and at 12 months or before restarting drug therapy. Seventy-four (70%) subjects had a potential follow-up of 12 months (four were withdrawn from the study) and 64 were available for two years of follow-up. Antihypertensive treatment was restarted if SBP > or = 160 mmHg and/or DBP > or = 90 mmHg on two consecutive visits. After 12 months, 20 (25%) of those withdrawn remained normotensive, the majority restarting therapy did so in the first three months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possibilities for antihypertensive drug therapy withdrawal in the elderly. 785 30

A randomized single blind cross-over trial with placebo lead-in has been conducted in 71 anginal patients with arterial hypotension (group 1) and 38 ischemic heart disease patients with normal arterial pressure (group 2) to compare efficacy of therapy with isosorbide dinitrate (ID), sustac-forte (SF), isosorbide dinitrate retard (IDR) and trinitrolong (TN). Paired bicycle exercises revealed that in group 1 patients ID was low effective in 49%, SF--in 61%, IDR was highly effective in 97% and TN--in 96%. In group 1 tolerance to antianginal effect of ID, SF and IDR shown by stress myocardial scintigraphy with Tl-199 developed earlier--in 2-4 weeks in 63-70% patients (versus 22-27% in group 2; p < 0.01). Recovery of ID, SF, IDR effect required prolongation of the drug withdrawal period to 8-16 days (versus 3-5 days in group 2; p < 0.05). TN therapy remained effective for 3 months. Resistance to ID, SF in group 1 was relative and depended on dosage form of nitrates.
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PMID:[Nitrates in therapy of effort angina in hypotensive patients]. 1468 13