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)

Our preliminary experience with dual-chamber DDD pacemakers is reported. Technological innovations of the device, atrio-ventricular electrode stability and sequential stimulation have contributed to improve the conditions of patients previously submitted to VVI pacemaker implantation. Primary indications for DDD pacemaker implantation in our series included 7 patients with complete atrio-ventricular (A-V) block, 3 with Mobitz type II second-degree A-V block and 2 with sick sinus syndrome. In six of the 12 patients (50%) additional indications included: ventricular tachycardia in 4 patients, atrial fibrillation in one and pacemaker syndrome in one. Other cardiac conditions were diagnosed: dilated cardiomyopathy in 3 patients, ischemic heart disease in 2 patients, valvular heart disease in 2 patients, congenital heart disease in 1 patient and hypertrophic cardiomyopathy in one patient. The implanted pacemakers were: 5 Genesis, 4 Ultra CPI and 3 Versatrax. J-shaped atrial electrodes were used in 8 patients and in 4 instances a screw-in electrode was employed. Improvement of hemodynamic function was achieved by frequent follow up and reprogramming of DDD pacemaker in every patient. While 4 patients died with progressive deterioration of cardiac function, eight patients survived with adequate sequential stimulation. We conclude that DDD pacemakers are reliable and afford symptomatic relief in a broad spectrum of patients.
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PMID:[DDD dual chamber pacemakers. Initial experience]. 134 19

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.
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PMID:The effects of acute and chronic cocaine use on the heart. 134 9

Anticholinergics (in particular, ipratropium bromide [Atrovent]) are first-line therapy in patients with chronic obstructive pulmonary disease (COPD). Although more studies are needed to support the use of combination therapy, adding an inhaled beta agonist to the therapeutic regimen is reasonable in patients who remain symptomatic and need quick relief. Patients frequently receive inadequate amounts of drug with standard doses delivered by metered-dose inhalers, often as the result of improper technique, so symptomatic patients may require higher doses. Caution is recommended when the dose of inhaled sympathomimetics is increased in COPD patients with ischemic heart disease or tachyarrhythmias. The addition of an oral sympathomimetic is seldom necessary. Theophylline may be considered in outpatients who remain symptomatic despite their use of inhaled bronchodilators, but heart disease, seizure disorders, and gastroesophageal reflux are contraindications. Corticosteroid therapy remains controversial but can be helpful in patients who still have severe disease despite maximum bronchodilator therapy. Antibiotics can be of benefit in COPD patients undergoing an exacerbation who have increasing dyspnea, cough, and phlegm production.
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PMID:Drug treatment of COPD. Controversies about agents and how to deliver them. 134 54

Ninety five patients with a mean age of 39 +/- 19 years, 82 of whom were symptomatic, having an accessory atrioventricular bidirectional conduction pathway (WPW syndrome: 77; "concealed": 18) were followed up for an average of 7.3 +/- 2.6 years. The objectives were to analyse: the incidence and causes of death and the possible predictive factors of death due to the WPW syndrome--the influence of medical treatment and type of medication on survival and symptoms. Of the 8 cardiac deaths, 6 seemed to be related to the WPW syndrome, a prevalence of 7.8% and an annual incidence of 1.1/1000. The main risk factors which were identified were: age 62 +/- 8 years versus 37 +/- 15 years in survivors; p < 0.02--associated organic heart disease, especially ischaemic heart disease (5/6)--the description of severe symptoms, in particular recurrent syncope--documented malignant spontaneous or induced arrhythmias (5/6)--anterograde AV conduction with an effective refractory period < or = 230 msec in 4, though it was only 270 msec in the other 2 patients, indicating that this parameter is not specific--amiodarone (6/6) did not prevent the fatal outcome in this particular group of patients. In the "benign" forms, only betablocker drugs could significantly reduce the frequency and severity of symptoms, especially when compared with Class I or IC antiarrhythmics. These results suggest that the indications of radical treatment should be widened in high risk patients, especially when elderly and with associated coronary artery disease. They also suggest that the role of betablocker drugs should be reevaluated in the so-called "benign" symptomatic forms.
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PMID:[Long-term outcome of a hospital series of patients with atrio-ventricular accessory pathway]. 136 71

Clinical, biochemical and epidemiological research has shown variations of serum enzymatic constellations (relatively high level of GGT in Chuckchi natives compared to nonnative newcomers). This difference leads to different unspecific body resistance to exogenous factors, particularly to histamine-liberators. The GGT system has also been linked to alcohol-induced clinical IHD. Based on these findings patients will be screened for GGT activity, which may serve as a marker for population phenotypes representative of high-risk groups. This deficiency in GGT may indicate a high risk for alcohol-related heart disease.
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PMID:Alcohol consumption and risk-factors for ischemic heart disease in Chuckchi inhabitants: clinical, biological and population studies. 136 79

Our purpose in this article is to examine the hypothesis that both myocardial disease and ischemia can alter the electrophysiologic function of the ion channels responsible for the cellular electrical activity of the heart. Changes in the intracellular and extracellular milieus occur during ischemia and can alter the electrophysiology of several species of ionic channels and the cellular electrophysiologic activity of cardiac myocytes. Included are 1) changes in extracellular [K+] and pH and in intracellular [Na+], [Ca2+], and pH; 2) accumulation of noxious metabolic products such as lysophosphatidylcholine; and 3) depletion of intracellular ATP. Finally, ischemia or disease (e.g., hypertrophy) can alter the electrophysiology of at least two types of K+ channels, the A-like channels underlying the transient outward current and the inward rectifier, by mechanisms that apparently do not involve alteration of either the intra- or extracellular milieus. Findings suggest that the expression of cardiac A-like channel function can be altered by hypertrophy and that at least one intrinsic conductance property of the inward rectifier can be altered by ischemia. We speculate that the control of expression, function, and regulation of cardiac ion channels can be affected at the molecular level by heart disease and myocardial ischemia.
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PMID:Connections: heart disease, cellular electrophysiology, and ion channels. 137 69

To explore whether exposure among firefighters to fire smoke could lead to an increased risk of cancer, lung disease, and heart disease, the mortality of 4546 firefighters who were employed by the cities of Seattle and Tacoma, WA and Portland, OR for at least one year between 1944 and 1979 were compared with United States national mortalities and with mortality of police officers from the same cities. Between 1945 and 1989, 1169 deaths occurred in the study population and 1162 death certificates (99%) were collected. Mortality due to all causes, ischaemic heart disease, and most other non-malignant diseases was less than expected based upon United States rates for white men. There was no excess risk of overall mortality from cancer but excesses of brain tumours (standardised mortality ratio (SMR) = 2.09, 95% confidence interval (95% CI) 1.3-3.2) and lymphatic and haematopoietic cancers (SMR = 1.31, 95% CI = 0.9-1.8) were found. Younger firefighters (< 40 years of age) appeared to have an excess risk of cancer (SMR = 1.45, 95% CI 0.8-2.39), primarily due to brain cancer (SMR = 3.75, 95% CI 1.2-8.7). The risk of lymphatic and haematopoietic cancers was greatest for men with at least 30 years of exposed employment (SMR = 2.05, 95% CI 1.1-3.6), especially for leukaemia (SMR = 2.60, 95% CI 1.0-5.4).
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PMID:Mortality among firefighters from three northwestern United States cities. 139 Feb 74

200 cases with the Qi Stagnation and Blood Stasis type of coronary heart disease were divided into two groups randomly. Group A used Rose Shu-Xin (heart comforting) oral liquid which is mainly made from the local natural resources-Rose compound products. While group B used Salvia miltiorrhiza (co.) tablet. The results showed that in group A, the total effective rate was 98% and the ECG improving rate was 75%, while in group B, it was 50% and 40% respectively. There was significant difference between group A and B (P < 0.01). Experiments have proved that the Rose oral liquid could improve the myocardial ischemia of the experimental rabbit. It could also reduce the size of infarction area, thus protected the heart from infarction. No adverse action was found in animal experiments and clinical practice. It has proved that the oral liquid could dredge the Liver and regulate the flow of Qi, and remove any obstruction to it. It could also promote the circulation of Blood and relieve pain. It gave the Heart disease a cure from the Liver in TCM theory.
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PMID:[Preliminary study of rose shu-xin oral liquid in the treatment of angina pectoris in coronary heart disease]. 139 93

The information explosion characteristic of recent years has presented a series of findings enabling a more effective prevention of ischemic heart disease by controlling low density lipoprotein (LDL) levels of cholesterol. The detection of LDL receptors has provided new information on the mechanisms regulating the level of plasma LDL. Data on competitive inhibitors of endogenous cholesterol synthesis have afforded new possibilities of pharmacological control of LDL levels. Studies of primary prevention of ischemic heart disease have yielded evidence showing that a 1% decrease of cholesterol level reduces coronary risk by 2%. A prospective study of the relationship between cholesterol levels and coronary mortality, absolutely unique as to its extent (368,000 middle-aged men followed up over a period of 6 years) has demonstrated that there is no borderline cholesterol level below which coronary risk would be absolutely excluded. Between total cholesterol level and coronary mortality there is a close, continual and graded relationship. In light of these findings, total cholesterol levels have been reclassified: desirable levels -5.2 x 10(-3) mol.l-1, borderline risk levels under 5.2-6.2 x 10(-3) mol.l-1, and high risk levels--above 6.2 x 10(-3) mol.l-1. In subjects with several risk factors (smoking, hypertension, familial occurrence of heart, heart disease, obesity, diabetes mellitus, HDL cholesterol below 0.9 x 10(-3) mol.l-1) the level of total cholesterol should be brought down below 4 x 10(-3) mol.l-1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Plasma cholesterol levels and ischemic heart disease: new findings and new approaches]. 139 27

A total of 53 patients with a provisional diagnosis of ischemic heart disease and without any clinical evidence of valvular, congenital, or primary muscle heart disease were studied by echocardiography and biplane left ventricular cineangiography. For angiographic ejection fraction analysis, a program developed in our department for use on an Apple Macintosh computer interfaced to a digitizing tablet was employed. Echocardiographic outlines of systolic and diastolic images were traced with a digitizing system on the screen and ejection fractions were calculated by a program incorporated in the echo machine. Good echo windows allowing ejection fraction calculations were present in 35 patients. There was a good correlation between angiographic and echocardiographic ejection fraction (r = 0.7, SEE = 0.09), and wall motion assessment revealed no significant discrepancies between the two image modalities. The remaining 18 patients had poor echo windows, preventing accurate echocardiographic determination of the ejection fraction. However, limited assessment of left ventricular size and wall motion was possible in all patients and allowed the identification of those who had impaired left ventricular function as judged by angiography (angiographic ejection fraction < 35%). We conclude that even in patients with poor echo windows echocardiographic assessment of left ventricular function provides clinical information similar to angiography which should not be considered mandatory for the investigation of ordinary ischemic patients.
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PMID:Is angiographic ventriculography necessary for the assessment of ischemic patients? 139 83


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