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)

Pressure overload hypertrophy of the left ventricle due to aortic stenosis is associated with abnormalities of left ventricular isovolumic relaxation and early diastolic filling. The relative contribution of the hemodynamic load on the left ventricle to the impairment of diastolic function observed in this disorder remains poorly understood. To study this relation, the vasodilator nitroprusside was administered to eight patients with aortic stenosis and normal systolic function. The effect of a short-term reduction in left ventricular preload and afterload on left ventricular isovolumic relaxation and early diastolic filling was assessed by analysis of simultaneous micromanometer left ventricular pressure and radionuclide angiographic volume measurements. At baseline, left ventricular systolic and end-diastolic pressures were markedly elevated, and associated with prolongation of the time constant of left ventricular relaxation and depression of the left ventricular peak filling rate. Infusion of nitroprusside resulted in reduction of left ventricular systolic (204 +/- 31 to 176 +/- 31 mm Hg, p less than 0.05) and end-diastolic (31 +/- 8 to 18 +/- 6 mm Hg, p less than 0.05) pressures, with no associated improvement in time constant of left ventricular pressure decay (T) (68 +/- 25 to 80 +/- 37 ms, p = NS), T 1/2 (34 +/- 8 to 34 +/- 14 ms, p = NS), left ventricular peak filling rate (2.3 +/- 0.5 to 2.3 +/- 0.8 end-diastolic volume/s, p = NS) or time to left ventricular peak filling rate (150 +/- 50 to 144 +/- 37 ms, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diastolic function in patients with aortic stenosis: influence of left ventricular load reduction. 296 27

Overt cardiac failure usually presents with constant clinical features as consequences of the reduced pump action, associated with an increased adrenergic drive, independent of the underlying disease. However, the study of left ventricular function, before and during the phase of cardiac insufficiency, shows that different pathophysiological mechanisms are responsible for the symptoms and signs of reduced cardiac action. It is possible to recognize that cardiac failure is caused primarily by: (1) early severe depression of the inotropic state, i.e. dilated cardiomyopathies; (2) late inadequate level of ventricular hypertrophy, with normal contractility, i.e. aortic stenosis; (3) early inadequate level of hypertrophy and slightly reduced inotropic state, i.e. mitral insufficiency, and (4) late inadequate level of hypertrophy and severe progressive reduction in contractility, i.e. aortic insufficiency. The possibility of an 'in vivo' assessment of the different determinant parameters of left ventricular function (contractility, afterload, preload, fiber and chamber compliance) through echocardiography enables a better understanding of the mechanisms leading to the cardiac failure and a more efficient therapeutic approach.
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PMID:Myocardial function in heart failure. 306 19

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

With the correct selection of drug and patient, the calcium antagonists as a group can be remarkably effective at relatively low cost of serious side effects. Almost all side effects are dose related. 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 (or diltiazem) 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 which actually has the most marked negative inotropic effect. Yet caution is required when even 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. The most marked interaction with digoxin is that with verapamil, which may raise digoxin levels by over 50%. Combination therapy of calcium antagonists with beta-blockers is increasingly common, and is probably safest in the case of dihydropyridines. Other combinations being explored are those with angiotensin-converting enzyme inhibitors and diuretics.
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PMID:Calcium channel antagonists. Part IV: Side effects and contraindications drug interactions and combinations. 315 4

Cardiac output and stroke volume were evaluated in 17 children (mean age 11.5 +/- 3 years) with discrete, membranous subvalvular (Group I, n = 7) and valvular (Group II, n = 10) aortic stenosis during submaximal and maximal (greater than 75% predicted maximal oxygen consumption) upright cycle ergometry. Patients with valvular aortic stenosis were further subdivided on the basis of their aortic valve gradient at rest determined by cardiac catheterization (Group IIA, gradient less than 40 mm Hg; Group IIB, gradient greater than or equal to 40 mm Hg). These patients were matched with 17 control subjects on the basis of age, sex, height and intensity of exercise during maximal exertion. Cardiac and stroke indexes were determined by the acetylene rebreathing method at each exercise level. Stroke volume index in Group I was significantly greater at rest when compared with that in control subjects (69 +/- 13 versus 53 +/- 11 ml/m2, alpha = 0.01, p less than 0.05) and that in patients in Group II (69 +/- 13 versus 47 +/- 12 ml/m2, alpha = 0.01, p less than 0.05). Patients with subvalvular aortic stenosis were unable to increase their stroke volume index from rest to submaximal exercise and also decreased their stroke volume index at maximal exercise levels. In contrast, patients with mild valvular aortic stenosis (Group IIA) displayed a normal exercise response. Patients with severe valvular aortic stenosis (Group IIB) had a blunted stroke volume response at rest and at each level of exercise, as well as signs of myocardial ischemia (ST segment depression) during maximal exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of the cardiac output and stroke volume response to upright exercise in children with valvular and subvalvular aortic stenosis. 334 67

As a result of improvement in intraoperative and postoperative management, severe aortic valve disease can be cured by operation, however, late cardiogenic sudden death after aortic valve replacement (AVR) has been existed as one of the important unsolved problem. This report is aimed to predict the risk factors influencing the postoperative prognosis of severe aortic valve disease. Twenty-three cases with aortic regurgitation (AR) and 20 cases with aortic stenosis (AS) were selected by postoperative period over 12 months. In 18 AR cases with normal coronary artery substantiated by selective coronary angiography, cross sectional area index of left ventricular wall (CSAI) and ST depression in left chest leads of electrocardiogram correlated well as the CSAI increased, so decreased the ST segment. This shows the increment of CSAI leads left ventricular endocardial ischemia. By means of introduction of this indicator, 23 AR and 20 AS patients were divided into two groups as group C-I having CSAI over 20 cm2/m2 and group C-II under 20 cm2/m2. Left ventricular ejection fraction (EF) was selected as an predictive indicator of left ventricular function. As same as CSAI, AVR cases were divided into two groups as group E-I having EF under 50% and E-II over 50%. Each group was compared concerning with the complication rate of postoperative low cardiac output syndrome (LOS) and late cardiogenic sudden death. In C-I group of AR, 55% cases accompanied with LOS, 18% died due to LOS and 18% died suddenly from late cardiogenic cause, however, none of cases in C-II group had these complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Risk factors influencing the prognosis of severe aortic valve disease following aortic valve replacement]. 369 58

In patients with valvar heart disease detection of coronary artery disease by conventional non-invasive methods may be difficult. The usefulness of thallium-201 exercise scintigraphy for detecting coronary artery disease was evaluated in 16 patients with aortic stenosis, 17 with aortic regurgitation, nine with mitral stenosis, and six with mitral regurgitation who were investigated by coronary angiography. Only two of 21 patients with greater than or equal to 50% coronary artery obstruction had normal thallium images. Three patients without angiographic evidence of coronary artery stenoses had perfusion defects demonstrated by thallium scintigraphy. Only one patient with greater than or equal to 75% coronary stenosis had a normal thallium scan. Angina pectoris or ST segment depression evoked by exercise test were not useful in distinguishing patients with coronary artery disease from those with normal coronary vessels. These data suggest that thallium exercise scintigraphy may be a useful non-invasive test for detecting coronary artery disease in patients with valvar heart disease.
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PMID:Detection of coronary artery disease by thallium scintigraphy in patients with valvar heart disease. 373 Feb 15

To evaluate the hemodynamic factors associated with treadmill-induced ST-segment depression in children with valvar aortic stenosis, 12 patients (mean age 13 years) with ST-segment depression during treadmill exercise and 5 patients (mean age 13 years) without ST-segment depression during treadmill exercise underwent exercise testing during cardiac catheterization. The left ventricular (LV) systolic pressure and LV outflow tract gradient at rest (177 +/- 25 vs 138 +/- 8 mm Hg and 59 +/- 18 vs 23 +/- 7 mm Hg, respectively) and corresponding pressures during maximal supine exercise (248 +/- 37 vs 189 +/- 17 mm Hg and 112 +/- 34 vs 52 +/- 14 mm Hg) were significantly greater (p less than 0.01) in the patients with exercise-induced ST-segment depression, although overlap existed. The LV-O2 supply-demand ratio during maximal supine exercise was significantly less (6.4 +/- 2.7 vs 11.8 +/- 0.7; p less than 0.005) in patients with than in those without exercise-induced ST-segment depression. In fact, an LV-O2 supply-demand ratio less than 11.0 was 100% sensitive and specific in predicting treadmill-induced ST-segment depression. These results suggest that although the development of ST-segment depression during treadmill exercise is related to LV systolic pressure and LV outflow gradient, its major hemodynamic determinant is the LV-O2 supply-demand ratio.
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PMID:Hemodynamic determinants of exercise-induced ST-segment depression in children with valvar aortic stenosis. 398 90

A 61 year old man with mild aortic stenosis and chronic depression took 12.5 mg digoxin in a suicide attempt. Ventricular tachycardia and fibrillation were resistant to lignocaine and to phenytoin but responded to intravenous amiodarone, with restoration of pacing. Because of persistent hyperkalaemia he was also treated with Fab fragments of digoxin specific antibody, which bound most of the ingested digoxin. It is suggested that the treatment of choice in severe digoxin poisoning is amiodarone for ventricular arrhythmias followed by pacing if necessary and the use of Fab antibody fragments if hyperkalaemia persists.
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PMID:Use of amiodarone and digoxin specific Fab antibodies in digoxin overdosage. 398 60

It is frequently stated that hypertrophied ventricles tolerate ischemia less well than nonhypertrophied ventricles. The authors' earlier studies in a rat supravalvular aortic stenosis model and canine valvular aortic stenosis model, both with concentric left ventricular hypertrophy, disclosed accelerated rates of ischemic contracture and diminished basal myocardial high energy phosphate stores. These studies have been extended to ten patients with severe left ventricular hypertrophy caused by valvular aortic stenosis and normal coronary arteries. ATP (endocardial and epicardial) from transmural left ventricular biopsies taken at operation before aorta cross-clamping, and frozen immediately in liquid nitrogen, were compared with similar biopsies from patients with nonhypertrophied myocardium supplied by normal coronary arteries. The subendocardial high energy phosphate levels in the nonhypertrophied myocardium was greater than high energy phosphate levels in the subepicardium of nonhypertrophied ventricles (ATP-micromoles/gram-protein, epi = 36.8 +/- 3.3, endo = 37.7 +/- 3.3) (p = NS). However, in the hypertrophied myocardium the subendocardium consistently showed significantly depressed high-energy phosphate levels when compared with subepicardial levels (ATP-hypertrophied myocardium, epi = 31.5 +/- 1.6, endo = 25.9 +/- 1.7) (p less than 0.05). This uniform depression of ATP stores, greatest in the subendocardium, in left ventricular hypertrophy suggests a common biologic mechanism for the enhanced sensitivity to ischemia. Of importance for patients may be the prior observation in rats that repletion of ATP( stores before ischemia eliminates the accelerated rate to ischemic contracture. Diminished subendocardial ATP stores appear to be an intrinsic property of severely hypertrophied myocardium and probably contribute to its enhanced sensitivity to ischemia.
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PMID:Depressed high-energy phosphate content in hypertrophied ventricles of animal and man: the biologic basis for increased sensitivity to ischemic injury. 621 20


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