Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fourteen patients, 2 to 20 years old were investigated. Two had primary pulmonary hypertension, 11 had congenital heart disease and post-tricuspid shunts, and 1, a 20-year-old patient, was investigated after he had undergone surgical correction of truncus arteriosus I. Pulmonary arterial pressure, pulmonary flow index, peripheral systolic blood pressure and heart rate were measured before, and several times after intrapulmonary injection into the pulmonary artery of 0.5 microgram nifedipine/kg. Six patients were given an additional dose of 1 microgram nifedipine per kilogram into the pulmonary artery and hemodynamic measurements were repeated. In eight children, receiving 100% oxygen via a breathing mask, nifedipine effects were compared with oxygen effects. After 10 minutes under oxygen, the same hemodynamics were determined as after nifedipine. In addition, in four of these children aortic pressure and arterial oxygen saturation were also measured. Maximal effects occurred within 4 minutes. 0.5 micrograms nifedipine per kilogram caused a slight reduction in mean pulmonary arterial pressure (p less than 0.05), as well as increase in pulmonary flow index (p less than 0.005). However, no significant change in heart rate or in systolic blood pressure was observed. 1 microgram nifedipine per kilogram IP had almost the same effects. No adverse side effects occurred, besides mild headaches in one child. A comparison of nifedipine injected into the pulmonary artery with oxygen breathing in congenital heart disease combined with pulmonary hypertension, is reported for the first time. Nifedipine had a more pronounced and beneficial effect with a selective action on the pulmonary vascular bed.
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PMID:Hemodynamic effects of nifedipine and oxygen in children with pulmonary hypertension. 315 41

The effects of long-term (mean 3.9 months) pharmacotherapy of hypertensive and normotensive hypertrophy (hypertensive heart disease, hypertrophic non-obstructive cardiomyopathy) as well as of advanced cardiac disease due to coronary artery disease and dilatative cardiomyopathy by large doses of nifedipine (mean 120 mg/day-1) were analyzed with regard to systolic blood pressure, to left ventricular function and to the hypertrophy degree of the ventricle. Nifedipine, in addition to conventional and maintained antihypertensive and cardiac therapy, lowers blood pressure in hypertensive patients, whereas hypotensive effects in the normotensive patients were absent. Nifedipine enhances left ventricular function in all patient groups significantly, i.e. in normotensive hypertrophic non-obstructive cardiomyopathy, in hypertensive heart disease and especially in heart disease due to coronary artery disease and dilatative cardiomyopathy. Significant regression of septal and of global hypertrophy was found in hypertrophic non-obstructive cardiomyopathy and in hypertensive heart disease. These results indicate, that long-term nifedipine treatment may be beneficial for left ventricular function in all patient groups and for hypertrophy regression in established left ventricular hypertrophy due to hypertrophic, non-obstructive cardiomyopathy and due to hypertensive left ventricular hypertrophy. It is concluded that long-term nifedipine treatment improves left ventricular function and leads to regression of established ventricular wall hypertrophy in hypertrophic non-obstructive cardiomyopathy and in hypertensive heart disease.
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PMID:Reversal of left ventricular hypertrophy and improvement of cardiac function in man by nifedipine. 624 3

The effect of nifedipine and nitroglycerin on the diameter of epicardial coronary arteries, the stenosis diameter, as well as arterial blood pressure and heart rate were recorded in 20 patients with coronary-heart disease. Nifedipine (20 mg sublingually) caused a significant fall in arterial pressure and a significant rise in heart rate. Additional administration of nitroglycerin (0.8 mg sublingually) caused a further fall in arterial pressure while heart rate remained constant. A definite relaxation (vasodilatation) of the epicardial vessels was demonstrated after nifedipine and a further increase after nitroglycerin. While nifedipine on average led to a significant increase in the diameter at the site of stenosis, response of individual stenoses was highly variable. In one patient with subtotal stenosis of the anterior interventricular branch a complete, transitory occlusion at the site of the stenosis occurred during nifedipine medication. This paradoxical reaction was not noted after nitroglycerin. Relaxation of the epicardial coronary arteries by nifedipine with suppression of phasic tone thus seems to be the major part of its anti-anginal effect. This effect is potentiated by nitroglycerin so that the combination of nitrate and calcium-antagonist appears to be therapeutically reasonable. In individual patients, however, there may be a paradoxical reaction to nifedipine.
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PMID:[Effect of nifedipine and nitroglycerin on epicardial vessels in coronary heart disease]. 642 31

Calcium ions have been shown to be involved in smooth muscle contraction and various secretory processes. Nifedipine, a calcium channel blocking drug, does not have any intrinsic bronchodilatory effect, but it has been suggested to possibly inhibit bronchial reactivity. Eight patients, with normal baseline pulmonary function studies and methacholine-induced bronchial reactivity, had a repeat metacholine challenge after nifedipine. Spirometry was obtained at baseline and three minutes after successive inhalations of normal saline and five, 15, 30, 50, 100 and 200 inhalation units of 0.5% methacholine. Plethysmographic lung volumes and airways resistance were measured at the start of the test and after the last inhalation of methacholine. The FEV1, FVC, MMEF and PEFR were reduced by an average of 35.6%, 20.6%, 54.4% and 30.6%, respectively, on the initial study, and by 35.4%, 20.5%, 54.8% and 34.5% after nifedipine. Airways resistance was increased by 249.3% in the initial study and by 265.7% after nifedipine. There was no statistical difference in baseline spirometry, spirometry obtained at any level of methacholine inhalation, or in airways resistance between the two studies. Despite comparable decreases in lung function, all patients were less symptomatic after receiving nifedipine. Nifedipine does not alter methacholine-induced bronchial reactivity. Until the role of nifedipine in asthma is better defined, caution should be used in prescribing nifedipine to asthmatic patients with heart disease, because their perception of airways resistance may be altered.
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PMID:Nifedipine does not alter methacholine-induced bronchial reactivity. 650 50

Nifedipine is a calcium antagonistic drug which reduces elevated vascular resistances. The hemodynamic effects of 20 mg of sublingual nifedipine were studied in 10 patients with chronic pulmonary hypertension. The etiology of pulmonary hypertension was chronic lung disease in 4, congenital heart disease in 2, mitral stenosis in 1, recurrent pulmonary embolism in 2 and primary pulmonary hypertension in one case. 30' after the drug administration there was a fall both of total pulmonary vascular resistance (from 992 +/- 586 to 648 +/- 428 d s cm-5, p less than 0.02) and of systemic vascular resistance (from 1416 +/- 868 to 896 +/- 440 d s cm-5 p less than 0.02) with an increase of systemic cardiac index from 3.2 +/- 1 to 4.5 +/- 2 l/min/m'2 (p less than 0.02). No significant change in systemic arterial oxygen saturation was noted, while pulmonary arterial oxygen saturation increased from 56 +/- 16 to 62 +/- 13% (p less than 0.01). These hemodynamic changes persisted for 120' when a significant fall of mean pulmonary arterial pressure was also noted (from 59 +/- 11 to 52 +/- 9 mm Hg, p less than 0.02). These data indicate that nifedipine may be useful to reduce pulmonary resistance in pulmonary hypertension. However this effect was less pronounced in patients with chronic lung disease compared to the other cases. It is suggested that the type of pulmonary arterial changes may determine the hemodynamic response. Nifedipine may be particularly indicated when vasoconstriction (as in primary pulmonary hypertension) is the main determinant of pulmonary hypertension.
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PMID:Hemodynamic effects of nifedipine in pulmonary hypertension. 716 46

Gingival hyperplasia caused by the use of nifedipine has been extensively reported. In this paper, the gingiva of 18 patients suffering from cardiopathy and treated with nifedipine were compared with those of 10 patients with cardiac disorders who had not been treated with calcium antagonists and with a no-treatment group of 12 patients. Nifedipine produced gingival hyperplasia, although patients who had not been treated with calcium antagonists also had mild hyperplasia. Hyperplasia first appeared in the interproximal areas, an observation which may be important for early detection. There was a direct correlation between the degree of hyperplasia and the bacterial plaque score. When we studied the influence of administration time and dose of nifedipine with the degree of hyperplasia, no statistically significant differences were found.
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PMID:Clinical assessment of gingival hyperplasia in patients treated with nifedipine. 819 41

Hypertensive crisis is a rare condition with increased blood pressure and evidence of new or progressive severe end-organ damage. The patients should be admitted to hospital, and the blood pressure reduced gradually. Blood pressure should not be normalized, but a reduction in mean arterial pressure of 20-25% or to a diastolic blood pressure > 100-110 mmHg should be achieved. Patients at particular risk for further complications are elderly, patients with hypovolaemia, renal insufficiency, ischaemic heart disease and patients with neurological deficits. The ideal antihypertensive drug for any form of hypertensive crisis does not exist. If the patient can cooperate with oral treatment, nifedipine may be used, usually administered as capsules of 10 mg orally, producing a rapid and safe reduction in blood pressure of 25% within 10-15 minutes with a maximal action after 30-60 minutes. The dose may be repeated after 30 minutes in case of insufficient blood pressure response. Hypotension is rare. Nifedipine in combination with nitroglycerine is of special benefit in hypertensive pulmonary oedema. In cases of treatment failure or if the patient cannot cooperate with oral treatment, the choice of drug lies between labetalol and sodium nitroprusside. Nitroprusside is administered as continuous intravenous infusion, the drug is safe to use and is recommended in conditions where reduction of blood pressure must be performed with extreme caution such as in cases of cerebral infarction and intracranial hemorrhage. Infusion of nitroprusside for more than 48-72 hours is inexpedient because the metabolites of nitroprusside need monitoring as well. Parenteral drug therapy with labetalol is more simple than treatment with nitroprusside, but at the same time somewhat more difficult to titrate. Nitroglycerine is very suitable in moderate hypertension and ischaemic heart disease, but in severe hypertension with heart disease nitroprusside is the treatment of choice. Loop diuretics should not be used as first-line drugs, but only in conditions with evidence of volume-overload. Patients with hypertensive crisis most often show volume depletion which is aggravated by loop diuretics, therefore they should not be used routinely. When the blood pressure has been stabilized, an oral antihypertensive drug should be started concomitantly to a gradual reduction of the initial parenteral drug therapy.
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PMID:[Hypertensive crises. 2. Treatment]. 875 95

Recent publications purporting to show that calcium antagonists, when used for the treatment of hypertension or in the post myocardial infarction patient, would paradoxically increase the rate of heart attack and mortality have cast doubts on the safety and efficacy of this drug class. All three studies are retrospective, and have various drawbacks. Specifically, the metaanalysis of Furberg et al is fraught with mistakes, of borderline significance, and based on old data pertaining to short-acting nifedipine only (which should not be given in patients who have suffered an acute heart attack). The case control study of Psaty et al suggested that hypertensive patients who were treated with short-acting verapamil, diltiazem, and nifedipine had an excessive rate of myocardial infarction when compared with patients who were treated with diuretics. Two out of the three calcium antagonists that were used in this study were not approved for the treatment of hypertension by the US Food and Drug Administration. Some patients were taking these drugs only once a day whereas, because of their short duration of action, at least a three or four times daily regimen would be required to achieve an acceptable blood pressure control throughout a 24-h period. The cohort study of Pahor et al suggested distinct differences among various calcium antagonists with regard to survival. Blood pressure was controlled in < 40% of all patients, and in some patients blood pressure was never even measured. Recent studies, such as the Prospective Randomized Amlodipine Survival Evaluation (PRAISE), the third Vasodilator-Heart Failure Trial (VHeFT-III), the second Doppler Flow and Echocardiography in Functional Cardiac Insufficiency Assessment of Nisoldipine Therapy (DEFIANT II), the Angina Prognosis Study in Stockholm (APSIS), and the Shanghai Trial of Nifedipine in the Elderly (STONE), attest to the safety and efficacy of the newer long-acting calcium antagonists in patients with a wide spectrum of heart disease. Several ongoing trials including the Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) with amlodipine, the International Nifedipine-GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT) with nifedipine, the Hypertension Optimal Treatment study (HOT) with felodipine, the Systolic Hypertension in the Elderly in Europe Trial (SYST-EUR) with nicardipine, the Second Swedish Trial in Old Patients with Hypertension (STOP II) with felodipine, and Nordic Diltiazem Study (NORDIL) with diltiazem, will give us morbidity and mortality data in patients with high blood pressure within the next few years. Until these results are available, we can be confident that the lowering of blood pressure and providing relief of patients with symptomatic angina can be achieved safely and efficiently with the presently available long-acting calcium antagonists.
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PMID:What, if anything, is controversial about calcium antagonists? 896 30

Cerebrovascular disease (CVD) is the third leading cause of death in United States and hypertension is a leading cause of both stroke and heart disease. It may cause headache, acute hypertensive encephalopathy, dementia and various types of strokes e.g., thrombotic, haemorrhagic, lacunar infarcts and transient ischaemic attacks. It remains the singlemost important treatable risk factor for stroke in all age groups and modern antihypertensive therapy has its documented prevention of stroke. Hypertension in acute phase of ischaemic stroke should not be treated. Hypertension in acute stroke should be treated. In advanced centres with specialised stroke units, the favoured drugs are short acting vasodilators e.g., sodium nitroprusside and labetalol. Nifedipine is the most popular drug followed by captopril, both sublingually and orally.
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PMID:Hypertension and cerebrovascular disease. 1064 96

The novel antihypertensive drugs which have been discovered and developed in the latter half of the 20th century were investigated. Newly discovered or improved drugs are approved by the Ministry of Health and Welfare in Japan, and after then they become available for clinical use. We can follow the progress and trends of various new antihypertensive drugs by recording their years of approval. The four primary useful drugs for the treatment of hypertension were developed were introduced as listed in the following: 1. Antihypertensive diuretics: Thiazide and dihydrothiazide were first approved in 1958, and various related drugs including aldosterone antagonists and loop diuretics followed. 2. beta-Adrenergic-blocking drugs: Propranolol was approved in 1966 for heart diseases and for hypertension in 1970. Thereafter many related drugs were developed. 3. Calcium channel-blocking drugs: Nifedipine was approved, for heart disease in 1974 and for hypertension in 1981, and then many related drugs appeared. 4. Angiotensin-converting enzyme inhibitors: Captopril was approved in 1982 and thereafter various related drugs followed. The four categories of these drugs were selected as first choice drugs for the treatment of hypertension in 1988. The development of these excellent useful drugs affected the mortality rates of cerebrovascular diseases (e.g., apoplexy). The mortality curve reaches plateaued in 1963, peaked in 1965, and then declined rapidly. Antihypertensive diuretic drugs stop the rise of mortality, and beta-blocking drugs, Ca-antagonists and ACE-inhibitors promote rapid downward tendency.
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PMID:[Fifty years history of new drugs in Japan: the developments and trends of antihypertensive drugs]. 1164 Feb 8


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