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)

The pathogenesis of cardiac arrest in the absence of any apparent heart disease remains unclear. Based on the hypothesis that coronary spasm may be a cause of cardiac arrest in the absence of apparent heart disease, ergonovine testing and/or electrophysiologic studies (EPS) were performed to evaluate the cause of cardiac arrest. Fourteen patients resuscitated from cardiac arrest had no apparent heart disease. A spontaneous episode of angina with ST-segment elevation occurred in 4 patients while under observation. Ergonovine testing was performed in 9 patients, and coronary spasm was induced in 5. EPS were performed in 8 patients, including 3 patients with coronary spasm. No electrophysiologic abnormalities were found in the 3 patients with coronary spasm. Ventricular fibrillation was induced by programmed ventricular stimulation in 2 patients with documented ventricular fibrillation at the time of resuscitation. All but one of the patients with coronary spasm had chest pain preceding cardiac arrest or at least a history of chest pain at rest, while 4 of 5 patients without coronary spasm had no prodromal symptoms. Patients with coronary spasm had a good prognosis when treated with a Ca-antagonist and/or long-acting nitrate. In conclusion, coronary spasm is the most frequent cause of cardiac arrest in cardiac arrest survivors with no apparent heart disease. Ergonovine testing should be performed to evaluate the cause of cardiac arrest when patients have no apparent heart disease.
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PMID:High prevalence of coronary artery spasm in survivors of cardiac arrest with no apparent heart disease. 841 43

Twenty outbreaks of Phalaris aquatica "sudden death" syndrome in sheep were investigated between 1981 and 1991. Four were confirmed and one was suspected, to be a cardiac disorder; 5 were confirmed and 3 were suspected, to be a polioencephalomalacic disorder; the aetiology of the remaining 7 outbreaks could not be determined. Potentially toxic levels of hydrocyanic acid (20 to 36 mg/100 g) were measured in the 3 toxic phalaris pastures tested. The measurement of potentially toxic levels of nitrate nitrogen (2920 micrograms/g) in toxic phalaris pastures by others, was noted. It is suggested that phalaris "sudden death" syndrome could have as many as 4 different underlying mechanisms, and that these might reflect the presence in the plant of a cardio-respiratory toxin, a thiaminase and amine co-substate, cyanogenic compounds, and nitrate compounds.
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PMID:Mechanisms underlying Phalaris aquatica "sudden death" syndrome in sheep. 144 81

Methemoglobinemia is a rare but easily diagnosed disease which may resemble cyanotic congenital heart disease. Toxic agents, mainly nitrate absorption, are often responsible and may reveal an underlying permanent or transient enzyme deficiency. Methemoglobinemia is of poor prognosis if secondary to hemoglobin disorders or congenital enzyme deficiency. Methylene blue is a good aid to diagnosis and a treatment of choice.
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PMID:[Non-cardiac cyanosis: methemoglobinemia in infants]. 164 40

We retrospectively studied all patients who had normal coronary angiograms at The Methodist Hospital during the year 1984 (8% of all angiograms). Patients were surveyed eight to 18 months after angiography. Of the 216 patients (83% of total sample), 130 were female and 86 male. Sixty-three percent of the women and 50% of the men satisfied the criteria for generalized anxiety disorder, and 20% satisfied the criteria for panic attacks. On the Brief Symptom Inventory (BSI) Somatization Scale, 64% had scores above the average reported for psychiatric outpatients. Eighty-one percent received only reassurance about the absence of heart disease, and 25% received continuing nitrate therapy in the absence of heart disease. A majority of these patients remain untreated functional "cardiac neurotics" with untreated anxiety symptoms. We make suggestions regarding a clinical profile to identify these patients and appropriate measures to avoid prolonged disability.
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PMID:Angina as a symptom of psychiatric illness. 290 61

We examined specimens from explanted human hearts by two-dimensional electrophoresis. The protocol selected includes: (a) solubilization of the sample in a urea-detergent mix; (b) charge fractionation in the presence of urea and nonionic detergent on a pH 4-10 immobilized pH gradient; (c) size fractionation on a polyacrylamide concentration gradient in the presence of sodium dodecyl sulfate; and (d) staining with silver nitrate. The method is sensitive enough for analysis of biopsies in the 1-3 mg range (wet tissue). We saw, for explanted hearts, variations in the protein pattern with the site of sample dissection. Results are presented for 11 explanted human hearts: one control organ and 10 pathological samples. The recorded pathologies included dilatative cardiomyopathy (six cases), valvulopathy (one case), ischemic cardiopathy (two cases), and graft rejection (one case). The patterns for whole extracts as well as for cytoplasmic proteins and myofibril components are compared. Extensive individual variability was observed both between control and pathological cases and among the abnormal samples.
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PMID:An examination of heart proteins by two-dimensional electrophoresis. 331 3

Pharmacological tests are often indispensable in non-invasive polycardiographic diagnosis. Their advantages include easy execution, repeatability, and the absence of significant side-effects. Amyl nitrate, angiotensin and isoproterenol are most commonly employed for this purpose. Cases in which such tests enabled a correct evaluation of valve disease, congenital heart disease, and malfunction of a valve prosthesis to be made are presented.
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PMID:[Pharmacological tests in the polycardiography of valve defects]. 611 41

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

The condition of hemomicrocirculation vessels in congenital heart disease was studied by silver nitrate impregnation of thick sections. Adaptive and pathological alterations in the microcirculatory bed of the heart in various developmental anomalies are described. The role of adaptive alterations of terminal vessels in an abnormal heart in the blood supply to hypertrophic myocardium is shown. It is suggested that pathological alterations in the microcirculatory bed of an abnormally for-med heart are associated with its functional over loading and weakening of coronary circulation. It is concluded that degenerative, focal destructive, and sclerotic processes in hypertrophic myocardium in congenital heart disease may depend on disturbances of microcirculation in the heart.
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PMID:[State of the blood microcirculatory vessels of the heart in congenital defects]. 644 95

Mammalian biological functions are organized according to circadian rhythms (lasting about 24 hours). They are coordinated by a biological clock situated in the suprachiasmatic nuclei (SCN) of the hypothalamus. These rhythms persist under constant environmental conditions, demonstrating their endogenous nature. Several genes of the circadian rhythm have been cloned in N. Crassa, Drosophilus and Mice, allowing molecular analysis of circadian functioning. Some rhythms can be altered by disease and drug pharmacology can be influenced by the time of their administration during the day (chronopharmacology). The rhythms of disease and pharmacology can be taken into account to modulate treatment over the 24-hour period (chronotherapy). The knowledge of such rhythms appears particularly relevant for the understanding and/or treatment of hypertension and ischaemic coronary artery disease. In rats and in man, the circadian rhythm of systolic or diastolic blood pressure can be dissociated from the rest-activity cycle, suggesting that it is controlled by an oscillator which can function independently of the SCN, which could justify modification of treatment according to the anomalies of the blood pressure rhythm. The morning peak of myocardial infarction in man is due to the convergence of several risk factors, each of which has a 24-hour cycle: blood coagulability blood, BP, oxygen requirements and myocardial susceptibility to ischaemia. The existence of these rhythms, and the chronopharmacology of cardiovascular drugs such as nitrate derivatives, constitute clinical prerequisites for the chronotherapy of heart disease.
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PMID:[Biological rhythms, chronotherapy and nitrates]. 945 77

Sildenafil citrate, an oral therapy for erectile dysfunction, is a selective inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5), the predominant isozyme metabolizing cGMP in the corpus cavernosum. Chemically, it is a compound of the pyrazolo-pyrimidinyl-methylpiperazine class. Sildenafil has no direct relaxant effect on human corpus cavernosum but enhances the relaxant effect of nitric oxide (NO) on the corpus cavernosum by inhibiting PDE5, which is responsible for degradation of cGMP in this tissue. When sexual stimulation causes local release of NO, inhibition of PDE5 by sildenafil increases concentrations of cGMP in the corpus cavernosum, causing smooth muscle relaxation and blood flow into the penis, resulting in an erection. Sildenafil at recommended doses has no effect in the absence of sexual stimulation. The drug is rapidly absorbed after oral administration, with absolute bioavailability of 40%. Its pharmacokinetics are dose proportional over the recommended dosage range. Maximum plasma concentrations are reached within 30 to 120 minutes after oral dosing in the fasting state. Sildenafil is cleared predominantly by the hepatic microsomal isoenzymes CYP3A4 (major route) and CYP2C9 (minor route). Clinical studies assessed the effect of sildenafil on the ability of men with erectile dysfunction to engage in sexual activity and, specifically, to achieve and maintain an erection sufficient for satisfactory sexual intercourse. Sildenafil was evaluated at doses of 25, 50, and 100 mg in randomized, double-masked, placebo-controlled clinical trials of up to 6 months' duration. The drug was administered to hundreds of patients aged 19 to 87 years having erectile dysfunction of various etiologies for a mean duration of 5 years. Sildenafil was associated with statistically significant improvement in erectile function compared with placebo. Adverse effects reported at a rate of >2% were headache, flushing, dyspepsia, nasal congestion, urinary tract infection, abnormal vision, diarrhea, dizziness, and rash. No cases of priapism were reported. The use of sildenafil is contraindicated in men who are taking organic nitrates, because of the potential for a precipitous decrease in blood pressure. Postmarketing reports and surveillance have revealed at least 39 deaths with sildenafil use in men having a history of heart disease, men taking nitrate medications, and men in poor physical health due to lack of exercise. Many of the men who experienced serious adverse effects or death had a variety of concomitant diseases and were taking multiple medications.
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PMID:Safety and efficacy of sildenafil citrate in the treatment of male erectile dysfunction. 991 1


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