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)

Medical critical care unit (MCCU) nurses at a VA medical center designed a quality assurance monitor for educating cardiac patients. Patients with a diagnosis of rule-out myocardial infarction are interviewed about their preadmission use of nitroglycerin and entry into emergency treatment facilities. The MCCU nurses teach a five-point "ischemic heart disease--recognition and response" lesson, and ascertain the patient's immediate level of understanding. If the patient returns to the MCCU at a later date, nurses record the appropriateness of his use of nitroglycerin and entry into emergency treatment facilities. Thus, both short- and long-term gains in patient knowledge are assessed. Solutions to problems encountered in the quality assurance monitor implementation process are discussed. Benefits of the project to patients, the nursing department, and other departments are identified. A sample monthly report and the monitor data collection tool illustrate the process. Future directions for patient education efforts in the MCCU are outlined.
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PMID:Patient education as a quality indicator in critical care: ischemic heart disease--recognition and response. 199 19

Although prostaglandin E1 is used to dilate the constricted ductus arteriosus in infants with cyanotic heart disease, the mechanism is unknown. To test the hypothesis that the cyclic nucleotides adenosine 3',5'-monophosphate (cAMP) and guanosine 3',5'-monophosphate (cGMP) play a role in relaxation, isolated rings of the ductus arteriosus of fetal lambs were studied. Tension of isometric contraction was measured by force displacement transducers. After contraction with oxygen, a control group was compared with rings in which the stimulus for relaxation was either nitrogen gas, prostaglandin E1 (PGE1), nitroglycerin (NTG), or nitroprusside (NPS). During relaxation, tissue was frozen at 30 seconds and at 1, 2, and 5 minutes and analyzed for cAMP and cGMP. PGE1 (10(-6) mol/L) decreased tension by 33% compared with 70% for nitrogen gas, 81% for NTG (10(-5) mol/L), and 92% for NPS (10(-5) mol/L). The maximal relaxation induced by PGE1 was associated with an 11-fold increase in cAMP; PGE1 had no significant effect on cGMP tissue levels. Nitrogen gas, NTG, and NPS produced similar increases in cAMP, and eight-, 25-, and nine-fold increases in cGMP, respectively. These results suggest that the patency of the ductus arteriosus is dependent on activation of both guanylate cyclase and adenylate cyclase and that the nitrovasodilators may be clinically useful in maintaining patency of the ductus arteriosus.
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PMID:Role of cyclic nucleotides in relaxation of fetal lamb ductus arteriosus. 303 77

In certain forms of congenital heart disease, patency of the ductus arteriosus is critical for survival. Since the administration of prostaglandin is associated with adverse side effects, this study was undertaken to evaluate the effects of nitroglycerin and nitroprusside on ductal blood flow during oxygen-induced ductal closure. Fifteen near-term fetal lambs were instrumented acutely. Ductal blood flow and pre- and post-ductal pressures were monitored continuously. After obtaining control data, intravenous bolus injections of nitroglycerin (250 micrograms), nitroprusside (250 micrograms), or prostaglandin E1 (5 micrograms) were administered during ventilation with either 100% nitrogen or 100% oxygen. All three agents significantly increased ductal blood flow during nitrogen ventilation (PO2 = 15 +/- 1 mm Hg). When the lambs were ventilated with 100% oxygen, the arterial PO2 increased to 107 +/- 14 mm Hg, and this was associated with a marked decrease in ductal blood flow from 275 +/- 44 to 83 +/- 11 ml/min (P less than 0.05). When nitroglycerin was administered during oxygen-stimulated ductal closure, ductal blood flow increased 184%, from 79 +/- 18 to 225 +/- 18 ml/min (P less than 0.05); nitroprusside increased ductal blood flow 126%, from 86 +/- 20 to 195 +/- 25 ml/min (P less than 0.05); prostaglandin E1 increased ductal blood flow 110%, from 84 +/- 18 to 178 +/- 17 ml/min (P less than 0.05). These data demonstrate that both nitroglycerin and nitroprusside are potent vasodilators of the ductus arteriosus and, like prostaglandin E1, can markedly attenuate the oxygen-induced ductal vasoconstriction. These results imply that nitroglycerin and nitroprusside may be useful clinically in maintaining ductal patency.
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PMID:Response of lamb ductus arteriosus to nitroglycerin and nitroprusside. 312 17

Twenty patients with congenital heart disease, ages 8 months to 6 years, received 1 to 5 micrograms/kg/min iv nitroglycerin after intracardiac repair to assess the hemodynamic effects of, and the pulmonary vascular response to, the drug in pediatric cardiac patients. Before surgery all patients had systemic-to-pulmonary blood flow ratios equal to or greater than 2.5:1. The pulmonary arterial pressure (PAP) was equal to aortic pressure in 14 patients and normal in six. The pulmonary vascular resistance (PVR) was elevated (more than 4 units) in five patients. After surgery, the right and left atrial pressures, PAP, and cardiac index were measured by thermodilution, and the systemic vascular resistance (SVR) and PVR were calculated. Intravenous nitroglycerin produced a significant drop in SVR at higher doses only (1602 +/- 359 to 1590 +/- 324 dynes X sec X cm-5, p = NS, at 2 micrograms/kg/min vs 1602 +/- 359 to 1247 +/- 417 dynes X sec X cm-5, p less than 0.01, at 5 micrograms/kg/min). Similarly, improvement in cardiac index was apparent only at higher doses (3.33 +/- 1.25 to 3.49 +/- 0.90 liters/min/m2, p = NS, at 2 micrograms/kg/min vs 3.33 +/- 1.25 to 3.82 +/- 0.98 liters/min/m2, p = NS, at 5 micrograms/kg/min). Also, the effect on the pulmonary vascular bed was most marked at higher doses and in patients with elevated PAP (175 +/- 27 to 148 +/- 28 dynes X sec X cm-5, p = NS, in patients with normal PAP vs 305 +/- 78 to 214 +/- 76 dynes X sec X cm-5, p less than .001, in patients with elevated PAP).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemodynamic effects of intravenous nitroglycerin in pediatric patients after heart surgery. 392 87

Traditionally when considering the pharmacologic basis of therapy in angina pectoris, attention is focussed on alterations of coronary blood flow. Yet the diseased coronary arteries in these patients often do not appear to be capable of responding to vasodilatory drugs. Since the pain of myocardial ischemia is relieved by a number of interventions without an increase in coronary blood flow, the concept herein considered is that angina pector is best viewed as an unfavorable relation between myocardial oxygen requirements and availability. Thus, the clinical value of the major antianginal agents is thought to be based importantly upon their actions to reduce myocardial oxygen consumption rather than to increase coronary blood flow. Sublingual nitroglycerin possesses a powerful dilator effect on veins which reduces venous return and thereby the size of the heart and intra-myocardial tension; thus myocardial oxygen requirements are diminished. The beta-adrenergic receptor blocking drug, propranolol (Inderal(R)), inhibits sympathetic stimulation of the heart at rest and during exercise. Thus, myocardial oxygen requirements are diminished by the reduction in heart rate and diminished contractility. As a result of this latter action, cardiac output is reduced and thereby arterial pressure and intramyocardial tension is lowered. In patients with advanced heart disease and borderline cardiac compensation, propranolol is hazardous because it removes the availability of one of the important reserve mechanisms for maintaining cardiac compensation-the sympathetic support of the failing heart. The introduction of electrical stimulation of the carotid sinus nerves as a means of therapy in patients with angina pectoris has provided a powerful tool for the treatment of patients with refractory ischemic pain.
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PMID:New trends in the treatment of angina pectoris. 498 Aug 81

A 62-year-old man who was under observation following an episode of severe chest pain developed complete heart block and hypotension after receiving sublingual nitroglycerin. The reaction occurred while the patient was receiving an intravenous maintenance infusion of lidocaine but did not occur in response to either nitroglycerin alone or lidocaine alone. There was no evidence of acute cardiac ischemia nor of clinically significant underlying heart disease. Complete heart block after sublingual nitroglycerin in the absence of significant cardiac disease is an exceedingly rare phenomenon.
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PMID:Complete heart block after sublingual nitroglycerin. 640 6

The temporal distribution and mechanism of death were studied in a large multicenter secondary prevention trial (Aspirin Myocardial Infarction Study) in which acute witnessed death represented 72% (270 of 376) of the deaths due to arteriosclerotic heart disease. Instantaneous deaths represented 28.9% (78 of 270) of the acute witnessed deaths; 45.2% (122 of 270) occurred in the first hour after the onset of symptoms and were defined as sudden deaths. In the subsequent 23 hours, an additional 113 deaths (41.8%) occurred and were defined as intermediate deaths; 29 late deaths (10.7%) occurred after 24 hours. Cardiac arrhythmia was the mechanism of death in 83% (194 of 235) of deaths within 24 hours. Univariate analysis of baseline clinical and electrocardiographic characteristics indicates that a history of congestive heart failure, cardiomegaly, angina pectoris, multiple myocardial infarctions and therapy with digitalis and nitroglycerin were more common in those who died than in survivors, regardless of the timing of death.
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PMID:Timing, mechanism and clinical setting of witnessed deaths in postmyocardial infarction patients. 642 16

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

In 12 patients aged from 45 to 75 years (mean : 62.57 +/- 8.37 years) a 2% percutaneous prepartion of nitroglycerin (PCNG) was applied on a square thoracic area measuring 15 x 15 cm, and its efficacy and duration of action were assessed by recording pressures in the right cavities and in the brachial artery. Left ventricular failure was due to recent myocardial infarction in nine cases, ischemic cardiopathy in two and non-obstructive cardiomyopathy in one. The 15 mg initial dose of PCNG was progressively increased until optimal dosage was reached. The efficacy of the drug was reflected in a significant fall in pulmonary artery diastolic pressure (PADP), equivalent to the mean capillary pressure, from 21.8 +/- 7.9 to 12.75 +/- 8.6 mmHg (p < 0.001). The mean systemic arterial pressure was reduced from 92.2 +/- 17.4 to 83 +/- 16.7 mmHg (P < 0.01). The cardiac index rose from 2.7 +/- 1 to 2.8 +/- 0.51/mn/m2 (N.S.) and the systolie index from 30.1 +/- 12.7 to 31.7 +/- 9.1 ml/systole/m2 (N.S.). Changes in PADP were significant (p < 0.05) during six hours and maximal at two hours (p < 0.001). There was a good correlation (r = 0.68 ; p < 0.02) between the time required to return to the initial values and the optimal fall in PADP. This shows that PCNG is undoubtedly long-acting in left ventricular failure, provided the doses are sufficient to induce a marked decrease in PADP.
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PMID:[Treatment of left ventricular failure with percutaneous nitroglycerin (author's transl)]. 677 2

Alterations in cardiovascular function induced by the acute intravenous administration of verapamil (5 or 10 mg) in 52 patients (29 with ischemic heart disease and 23 without heart disease) were evaluated with use of invasive techniques (right and left heart catheterization, left ventricular cineangiography, and coronary arteriography). The most significant changes were represented by a decrease in systemic vascular resistance and systemic arterial pressure, and an increase in heart rate and cardiac output. Contractility indexes were not depressed in either group, and altered ventricular wall motion tended to improve to a slightly smaller degree than in patients treated with nitroglycerin. The use of verapamil in patients with ischemic heart disease appears to be safe, and concern about the negative inotropic influences in humans no longer seems justified.
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PMID:Changes in cardiovascular function induced by verapamil in healthy subjects and in patients with ischemic heart disease. 722 86


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