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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most of type 2. diabetic patients require medication for several concomitant diseases, most important being, hypertension, ischaemic heart disease, heart failure, dyslipidaemias, obesity. Thus the risk of drug interactions is important, particularly in elderly patients. Oral antidiabetic drugs include hypoglycaemic agents (sulphonylureas, meglitenides) and biguanides (metformin), alpha-glucosidase inhibitors, tiazolinidediones. Drug interactions with antihyperglycaemic agents can be divided into pharmacokinetic and pharmacodynamic interactions. Numerous drugs due to interactions enhance hypoglycaemic action of sulphonylureas, thus increase the risk of hypoglycaemia. Several drugs may cause impairment of glycaemic control through various mechanisms in diabetic patients treated with oral antidiabetic drugs. Currently the most controversial problem is safety of combination therapy with sulphonylurea and metformin, as several observations indicated that it can increase mortality from cardio-vascular causes.
Pol Merkur Lekarski 2000 Sep
PMID:[Clinically important effects of oral antidiabetic drug interactions]. 1112 85

Cor pulmonale is defined as "hypertophy of the right ventricle resulting from diseases affecting the function and/or structure of the lungs, except when these pulmonary alterations are the result of diseases that primarily affect the left side of the heart, as congenital heart disease". Pulmonary hypertension is a frequent hemodynamic complication associated with a wide variety of respiratory systems disorders whose only common physiologic abnormalities are alveolar hypoxia and consequent arterial hypoxemia of longterm duration. The sustained elevation in pulmonary arterial hypertension is thought to be mediated through two pathophysiologic vascular mechanism: 1) persistent vasoconstriction and 2) vascular structural remodeling. The combination of these processes causes vascular luminal narrowing and vessel obliteration that reduce pulmonary vascular surface area to the critical degree necessary for the development of the pulmonary hypertension. Cor pulmonale may be difficult to diagnose, particularly early in its course, when they symptoms manifested may be interpreted as representing progression of an underlying pathophysiological state, such as chronic obstructive airways disease. The treatment of cor pulmonale is directed toward reversing the pathogenetic process that can be directly treated, while at the same time relieving the hypoxemia, hypercapnia or acidosis. At present long-term oxygen therapy is the best treatment for pulmonary hypertension. Heart failure in cor pulmonale is usually transient once the initiating mechanism is controlled. The usual therapeutic measures for heart failure apply: a low-salt regimen, and diuretics.
Pol Merkur Lekarski 2000 Oct
PMID:[Chronic cor pulmonale]. 1114 67

We have reported twin pregnancy complicated by uncommon "twin reversed arterial perfusion" syndrome. Ultrasound scan at 27th week of gestation revealed one normal foetus and the second one "acardiac" with severe malformations. Since the cardiac failure of the first twin was observed, the digitalis were administered till the end of pregnancy. The pregnancy was terminated at 31st week by caesarean section. We succeed in delivering one healthy newborn, which was possible by appropriate management including elective termination, observation (ultrasonography and cardiotocography) and nonsurgical intervention (digitalis).
Ginekol Pol 2000 Nov
PMID:[Twin pregnancy complicated by "twin reversed arterial perfusion" syndrome]. 1121 49

The subject of this study was a group of 757 patients hospitalized because of acute myocardial infarction in years 1992-1996, who survived the in-hospital course and were under observation for 2-6 years after the infarction. During the 14-18th day of the hospital stay they were made an echocardiographic test, including the ejection fraction (EF). The aim of this study was to define the influence of the ejection fraction value lowered below 40% on the long-term prognosis in patients after acute myocardial infarction. We compared two groups of patients; group I, consisting of 130 (17.2%) patients with EF lowered below 40% and group II, which included 627 patients with EF over 40%. To estimate the statistic significance we used the chi-square and t-Student test. The morbidity curves were made with the Kaplan-Meier method. The course of the myocardial infarction was much more grave in group I than in group II, what is confirmed by a more often anterior ventricular infarction and the quantity of dangerous complications which occurred during the in-hospital phase. The multi-factor regressive analysis showed that the ejection fraction lowered below 40% raises 2.47 times (95% confidence interval 1.50-4.07) (p < 0.001) the risk of death during the first year after myocardial infarction and nearly two times during the 5 year follow-up, compared to patients with a higher EF value. The influence of the EF value lowered below 40% on the creation of an infarction was not significant. The EF value lowered below 40% in patients after acute myocardial infarction was a significant risk factor in the long-term prognosis. More than 40% of deaths during the long-term prognosis in this group were caused by heart failure.
Pol Arch Med Wewn 2000 Jul
PMID:[The significance of lowered ejection fraction on prognosis after myocardial infarction ]. 1130 28

From the group of 66 patients (pts) treated with in-hospital haemodialysis (HD), 30 pts were selected for 48 hrs monitoring of heart rhythm to register arrhythmias using Holter method. Cardiovascular complications were observed in 24 pts (80%) of the studied group; ischemic heart disease in 10 pts (33%), chronic cardiac failure in 8 pts (27%), left ventricular hypertrophy in 16 pts (53%) and hypertension in 24 pts. During 48 hrs of heart rhythm monitoring ventricular heart arrhythmias (VHA) were registered in 23 pts. 8 pts of this group had more then 100 additional ventricular beats for 24 hrs. VHA were registered before HD in 14 pts, during HD in 15 pts and after in 15 pts. The frequency of VHA pt/one hour of monitoring increased during and immediately after HD. There were no statistically significant differences between 23 pts with VHA and 7 pts without VHA with respect to the following parameters measured before HD: blood pressure, urea, calcium, kalium and magnesium blood concentrations. We found statistically significant difference between both groups of pts for creatinine values (p < 0.02); respectively 899.7 mmol/l SD 152 mmol/l versus 767 mmol/l SD 95.3 mmol/l and for interdialytic body weight increase (p < 0.012); respectively 2.65 kg SD 0.8 kg versus 2.04 kg SD 0.46 kg. Our initial results indicate that VHA appears in the majority of hemodialysed pts and that HD intensifies arrhythmogenic influence of irreversible renal failure on heart. It is also possible that non-adequate HD might be responsible for induction of ventricular heart arrhythmias during and after dialysis.
Pol Arch Med Wewn 2000 Oct
PMID:[Ventricular arrhythmia in patients with chronic renal failure treated with hemodialysis]. 1139 59

Many clinical aspects associated with chronic uraemia and long-term dialysis therapy may determine both the qualification for renal transplantation and post-transplant outcome. These include dialysis access, severe hyperparathyroidism, inadequate or excessive erythropoietin production, heart failure, viral hepatitis, defects of urinary tract and malnutrition. Some of them delay the qualification for transplant, the other on contrary make the need for transplantation very urgent. Selected aspects are discussed in this paper.
Pol Merkur Lekarski 2001 Apr
PMID:[Patients on dialysis as renal graft recipients]. 1143 86

Neuropeptide Y (NPY) has been recently characterised as one of the strongest circulating vasoconstrictor peptides, its elevated level may cause coronary artery spasm and increase of peripheral vascular resistance. All this contributes to ischemic myocardial damage and decrease of regional and global left ventricular function. The aim of the study was the examination of NPY plasma levels in patients with acute myocardial infarction (AMI) after thrombolytic therapy with or without reperfusion. The survey was made in 82 patients with AMI after thrombolytic therapy: 40 of them without reperfusion and 42 with reperfusion. The control group consisted of 20 healthy persons. Plasma levels of NPY were measured before thrombolysis, then 1, 3 and 5 days after, using a radioimmunologic method. All patients were treated with aspirin, glyceryl trinitrate and thrombolytic therapy (TT) with alteplase (r-TPA). In patients with AMI, NPY plasma levels were normal before and 1 day after TT, and were significant elevated 3 days after TT 5 days after TT, plasma NPY levels were still high in patients without reperfusion, but they decreased in patients with reperfusion. There was significant negative correlation between NPY level and left ventricular ejection fraction measured 5 days after AMI. During 30-days follow up systolic dysfunction of left ventricle with ejection fraction under 40% occurred in 21 patients and in 11 of them clinical symptoms of heart failure were observed. Using the multivariable regression analysis we showed that NPY concentration over 60 pg/ml is the independent factor leading to left ventricle systolic dysfunction. The results of our study suggest the contribution of NPY to the left ventricular remodeling after AMI.
Pol Arch Med Wewn 2001 Feb
PMID:[Plasma levels of neuropeptide Y i patients with current myocardial infarction]. 1150 45

61 years old man with 30-years history of ankylosing spondylitis was admitted to hospital because of respiratory and cardiac failure. Chest X-ray and CT scan showed nonspecific inflammation but microbiological diagnosis allowed to establish the diagnosis of pulmonary tuberculosis. During antibioticotherapy and antituberculous treatment respiratory failure regressed.
Pneumonol Alergol Pol 2001
PMID:[Pulmonary tuberculosis during a course of ankylosing spondylitis]. 1157 4

In the last few years medical genetics is assuming a much more prominent position in the etiology of cardiac diseases. The article presents the current state of the molecular and genetic basis of diseases leading to heart failure, such as coronary artery disease, idiopathic cardiomyopathy, valvular abnormalities, essential hypertension and other rare cardiac diseases. Looking for the molecular basis is followed by practical advice on the role of genetic testing, expanding of the methods of prophylaxis, modification of medical managing and treatment.
Pol Merkur Lekarski 2001 Jul
PMID:[Genetic basis of cardiac diseases leading to heart failure]. 1157 32

QT dispersion reflects in homogenecity of ventricular repolarization. It is calculated using 12-leads standard synchronized ECG or 24-hours Holter monitoring. The most common used indicators are: QT dispersion (QTd), based on Bazett's formula corrected for heart rate QT dispersion (QTcd) and QT dispersion ratio (QTdR). QT apex and QTd corrected for total number of leads ECG in which QT interval was counted are rare used. Increased QT dispersion is observed among others: following myocardial infarction (MI), coronary heart disease (CAD), hypertension, chronic heart failure (CHF), long QT syndrome, as well as diabetes. Following mentioned diseases increased QT dispersion has prognostic value for sustained ventricular tachycardia. Dispersion of repolarization > or = 80 ms after MI is a risk factor for sudden cardiac death. Following acute MI decrease of QT dispersion after successful thrombolytic therapy is observed and its value > or = 100 ms is regarded as a marker of reperfusion insufficiency. QT dispersion in patients with CAD correlates with extent of ischemia and decreases after coronary angioplasty (PTCA). In recent years beneficial effect of angiotensin-converting enzyme inhibitors and beta-adrenolytic therapy on QT dispersion was described. Actually the improvement of computerised methods in assessment of QT dispersion is observed, but it require further investigations.
Pol Merkur Lekarski 2001 Jul
PMID:[Measurement dispersion of the QT interval and its significance in different diseases]. 1157 33


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