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Biomedical subjects

S Cagan

Publications and source records attributed to S Cagan.

8 recordsLinked to original sources
PubMed1998

[In Process Citation]

Project Audit of diagnostic and therapeutic procedures in patients with acute coronary syndromes was approved by the Ministry of Health of the Slovak Republic on 13 May 1996. The essence of the project resides in a systematic and complex analysis of quality of provided medical care and the use of sources with the seeking for possibilities of improvement of the provided care aimed at prognosis and quality of life of patients with acute coronary syndrome (acute infarction, unstable angina pectoris, sudden cardiac death). The subsequent step will reside in the Project of Sudden Cardiac Death Prevention and the establishment of the myocardial infarction register.

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PubMed1998

[In Process Citation]

Diabetes mellitus type 2 (DM type 2) is a common disease that is associated with high mortality and morbidity due to macrovascular and microvascular complications. CHD mortality and morbidity is 2--3 times higher in diabetic than in non-diabetic patients/. There are many potentially atherogenic factors in diabetes these may underlie this problems. Except major risk factors (high serum cholesterol concentration, hypertension, cigarette smoking), insulin resistance is common in DM type 2 patients. The dyslipidemic component of insulin resistance is "atherogenic lipoprotein phenotype", its components include small LDL particles (pattern B) with higher atherogenic risk. Several recent studies have demonstrated the preponderance of small, dense LDL in patients with DM type 2 and IR. The question of whether small, dense LDL can be explained by triglyceride levels alone or whether it is directly related to DM type 2 and insulin resistance is still the subject of debate. If serum triglycerides exceed 1,3 mmol/l, small, dense LDL increases. The practical implication is that serum triglyceride levels should be maintained as low as possible to prevent the deleterious effects of triglycerides on LDL subclass distribution and size. There are several potential mechanisms to explain the increased atherogenicity of dense LDL (small dense LDL is more susceptible to lipid peroxidation and oxidation leading to its increased uptake by macrophages and subsequent removal by scavenger pathway, also has a lower binding affinity to LDL receptors). Theoretical grounds postulate that the treating of diabetic dyslipoproteinemias would reduce atherosclerosis disease. However, to date, there have been no intervention studies specifically designed to test this postulate in the diabetic population Such studies the Diabetes Atherosclerosis Intervention Study (DAIS), Fenofibrate Intervention and Event Lowering in Diabetes (FIELD), Collaborative Atorvastatin in Diabetes Study and lipid in Diabetes Study are currently in progress (Tab. 4, Fig. 2, Ref. 81.).

Journal Article↗
PubMed1998

[In Process Citation]

Reperfusion arrhythmias originate as a consequence of the complex of cellular and humoral reactions accompanying the opening of coronary artery. As the primary cause of their generation are considered the chemically defined substances that are produced and accumulated in myocardium during reperfusion. The key role id ascribed to free oxygen radicals but of importance are also other substances such as calcium, thrombin, platelet activating factor, inositol triphosphate, angiotensin II and others. These chemical mediators of reperfusion arrhythmias operate as modulators of cellular electrophysiology causing the complex changes at the level of ion channels. It is supposed that in the genesis of reperfusion arrhythmias unlike ischemic arrhythmias operate nonreentrant mechanisms such as abnormal or enhanced automacy and triggered activity due to afterdepolarizations. As a typical reperfusion arrhythmia is considered an early (within 6 hours after start of thrombolysis), frequent (> 30 episodes/hour) and repetitive (occurring during > 3 consecutive hours) accelerated idioventricular rhythm (AIVR). AIVR with such characteristics has a high specificity and positive predictive accuracy but relative low sensitivity as a predictor of reperfusion. Thus, in occurrence of AIVR, recanalization of infarction-related coronary artery is very probable, but in absence of AIVR, reperfusion is still not excluded. The following arrhythmias are regarded also as markers of reperfusion: frequent premature ventricular complexes (> twofold increase in frequency within 90 minutes after the start of thrombolysis), a significant increase of episodes in nonsustained ventricular tachycardia, sinus bradycardia and probably also high degree atrioventricular blocks. At present, there is no definite evidence, as to whether sustained ventricular tachycardia and especially ventricular fibrillation can be caused by reperfusion. Reperfusion arrhythmias are an important noninvasive marker of successful recanalization of infarction-related coronary artery. However, they are also a sign of reperfusion injury and a finding which may limit the favourable effect of reperfusion. In account of that, there is a very intensive search for pharmacologic interventions which could protect or attenuate the reperfusion injury and thereby also the genesis of reperfusion arrhythmias. Although promising results were obtained with many substances antagonizing the effects of mediators of reperfusion injury, there is no definite recomendation for their use under clinical conditions. However, the results from the latest clinical trials with ACE inhibitors are very promising. These trials render relative conclusive evidence, that ACE inhibitors could have a protective effect against reperfusion arrhythmias. (Ref. 89, Tab. 1.)

Journal Article↗
PubMed1998

[In Process Citation]

In addition to ventricular arrhythmias, various forms of supraventricular arrhythmias (SVA) and atrioventricular (AV) and intraventricular (IV) conduction disturbances occur also in acute myocardial infarction (AMI). In the setting of AMI, SVA may be caused by relevant atrial ischemia or infarction. SVA complicate the course especially that of inferior, posterior and lateral AMI, SVA occur frequently also in the right ventricular myocardial infarction and in pericarditis. SVA appearing in the late phase of AMI are caused particularly by hemodynamic factors especially those of both left and right ventricular dysfunctions. Atrial dilatation and the increase of intraatrial pressure are also important factors in the genesis of SVA. The autonomous nervous system, electrolyte disturbances, acidosis and global hypoxia may operate as modulating factors in the development of SVA. AV conduction disturbances are significantly more frequent in patients with inferior than with anterior AMI. In inferior AMI, they are frequently caused by reflex parasympathetic activation. In the genesis of AV conduction disturbances, a significant role may be played also by the following mechanisms: Ischemia or necrosis of AV node or AV junction and the negative dromotropic effect of adenosine and potassium which are released to a great extent during myocardial ischemia and reperfusion. A high-degree AV block complicating the course of inferior AMI has a significantly better prognosis than that occurring in the setting of anterior AMI. In inferior AMI, AV block is frequently reversible, whereas in anterior AMI, it is persistent and irreversible. Early AV conduction disturbances, appearing within 24 hours of AMI have a better prognosis than those occurring in the late phase of AMI. Bundle branch blocks (BBB) complicating the course of AMI are caused by occlusion of bundle-related coronary artery or by serious ischemia in its bed. BBB is frequently a marker of a multivessel disease. New BBB appearing in AMI especially the right bundle branch block is considered as an predictor for the development of a complete AV block. Frequent and repetitive SVA as well as serious AV and IV conduction disturbances are frequently associated with a significantly worse clinically course of AMI and with increased mortality, with that of especially hospital mortality. However, this is usually not caused by SVA or AV and IV conduction disturbances per se. The major cause of death in these patients are heart failure cardiogenic shock and malignant ventricular arrthythmias due to larger AMI, significant reduction of left ventricular function and advanced coronary heart disease. Complex SVA as well as serious AV and IV conduction disturbances are usually considered as markers, but not as independent predictors for both increased hospital mortality and in some cases also for that of posthospital mortality. Their occurrence in AMI may help to identify the patients at great risk who require a very intensive treatment including aggressive management of extensive coronary heart disease. (Ref. 62.).

Journal Article↗
PubMed1998

Informacia o niektorych vysledkoch z Pilotnej studie projektu Ministerstva zdravotnictva SR. AUDIT diagnostickeho a terapeutickeho postupu u chorych s akutnymi koronarnymi syndromami

The basic analysis of the Pilot study fully confirms the possibilities of the realization of the project AUDIT ... in the planned form, the necessity to realize this project regarding the discovery of several negative facts in the management of patients with AMI, which can affect infavourable the course of the disease in patients with AMI and their prognosis or unjustifiably increase the economic impact. The most severe of them are investigated in this information and we present them in subsequent order of individual phases of the management of patients afflicted by AMI.

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