Biomedical subjects

B Swidnicka-Szuszkowska

Publications and source records attributed to B Swidnicka-Szuszkowska.

4 recordsLinked to original sources

PubMed2001

[Effect of digoxin on atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and cyclic 3', 5'-guanosine monophosphate (cGMP) in patients with chronic congestive heart failure].

UNLABELLED: Neurohumoral factors play important role in the pathogenesis of congestive heart failure (CHF) and digoxin (dig) is one of the most frequently used drugs in this condition. The aim of this study was to assess the effects of dig on atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and their "second messenger" cyclic 3',5'-guanosine monophosphate (cGMP). MATERIAL AND METHOD: The study group consisted of 25 patients (pts) aged 25-81 with CHF (NYHA II/III), 13 women and 12 men. Control group consisted of 10 healthy volunteers, 2 women and 8 men. The blood samples for evaluation of ANP, BNP and cGMP plasma level was taken at baseline conditions and 3 hours (h) after intravenous injection of 0.25 mg of dig. From the next day 0.25 mg dig was administrated orally for 6 days and plasma levels of ANP, BNP and cGMP were assessed on the 3rd and 6th day of treatment. Medium serum dig concentration on the 6th day was 0.98 ng/mL. RESULTS: The baseline ANP, BNP and cGMP plasma level was significantly higher in pts with CHD than in control group (ANP 144.4 vs 98.8 pg/ml p < 0.001; BNP 130.0 vs 97.2 pg/ml p < 0.001; cGMP 1.44 vs 0.86 pg/ml p < 0.001). In pts with CHF there was a significant increase ANP, BNP and cGMP plasma level 3 h after dig intravenous injection (ANP 205.2 vs 144.4 pg/ml p < 0.01; BNP 227.1 vs 130.0 pg/ml p < 0.01; cGMP 1.84 vs 1.44 pg/ml p < 0.01). The ANP and BNP plasma level after 3 days of oral dig was still significantly increased (ANP 171.1 vs 144.4 pg/ml p < 0.05; BNP 223.7 vs 130.0 pg/ml p < 0.01). ANP, BNP and cGMP plasma level was higher in pts with CHF also after 6 days of oral dig, but the difference was statistically significant. After 6 days of digoxin treatment there was a significant increase of ejection fraction (p < 0.005), with reduction of end-diastolic diameter of left ventricle (p < 0.05) and diameter of left atrium (p < 0.01). ANP at baseline correlated positively with baseline cGMP (r = 0.702 p < 0.05). On the 6th day BNP correlated positively with cGMP (r = 0.628 p < 0.05). 3 h after dig intravenous injection ANP correlated positively with BNP (r = 0.881 p < 0.05), but on the 3rd day of oral dig ANP correlated negatively with BNP (r = -0.536 p < 0.05). On the 6th day of oral dig end-diastolic diameter of left ventricle correlated negatively with BNP (r = -0.483 p < 0.05) and cGMP (r = -0.824 p < 0.05). CONCLUSIONS: 1. In pts with CHF a single intravenous digoxin injection increases ANP, BNP and cGMP plasma level. 2. Oral digoxin administration supports this beneficial neurohumoral effect and improves hemodynamic parameters of left ventricle as well as reduces left atrium diameter.

Administration, Oral↗

PubMed2000

[Chronic cor pulmonale].

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.

Chronic Disease↗

PubMed1999

[Silent myocardial ischemia].

Silent myocardial ischemia (SMI) is a manifestation of coronary artery disease in which persons have episodes of myocardial ischemia that are not accompanied by chest or anginal pain. Episodes of SMI have been described as the predominant form of transient myocardial ischemia in patients with stable angina, those with unstable rest angina and even variant angina. Silent myocardial ischemia is also known to occur in some patients with myocardial infarctions and resuscitated from episodes of sudden cardiac death, thus occur frequently in patients with all of the usual symptomatic phases of coronary artery disease. A number of studies have now clearly demonstrated that patients with silent ischemia have increased risk for coronary events: sudden death or myocardial infarction. SMI is most often recognized during exercise testing or fortuitously with ambulatory electrocardiography. For today it is imperative to investigate every patient in whom multiple risk factors of IHD have been recognised, even in the absence of chest pain. The early detection of SMI may help to prevent later cardiac events. If the ischemia (symptomatic and silent) itself is the cause of the higher mortality rate, then the goal of therapy should be to abolish it either by pharmacological means or by invasive interventions as balloon angioplasty or coronary bypass surgery.

Electrocardiography↗

PubMed1998

[Pharmacological treatment of lipid disorders according to present clinical studies].

Hyperlipidemia beside hypertension, diabetes mellitus and smoking, is considered as the most serious factor of atherosclerosis. Studies performed in Poland indicated that only 28% of men and 32% of women has proper lipids concentration in blood serum. In 1992 the European Atherosclerosis Society (EAS) divided hyperlipoproteinemia into three types: hypercholesterolemia, hypertriglyceridemia and mixed hyperlipidemia, and each of them into mild and significant. Starting treatment attention should be paid not only on kind of lipid disorders, degree of its intensity, but also there should be evaluated other existing risk factors. Priority in treatment of hyperlipidemia consist of patients with established coronary heart disease and other forms of atherosclerotic disease. Clinical studies of last years for example like CARE, 4S, LCAS indicated plenty of advantages of lipid-lowering therapy in this group of patients, resulting in reduction total mortality coronary mortality, and recurrent coronary events. Second group consist of patients without clinical atherosclerotic disease, with high risk category. Advantages of lipid-lowering therapy in primary prevention resulting in reduction of coronary heart disease frequency proved between others study: LRC-CPPT, Oslo Study, WOSCOPS. Another groups consist postmenopausal women, in whose estrogen replacement therapy has an effect not only on improvement of lipides parameters, but also has beneficial effect on vassals endothelium and reduces risk of heart coronary disease down to 50%. Finally, there was described also problem of hypercholesterolemia treatment in young and older patients. New trends in treatment of lipid disorders were also presented.

Aged↗