Thrombosis in ischemic heart disease

Thrombus formation on a fissured or disrupted atherosclerotic plaque is the main pathogenetic mechanism for the acute coronary syndromes of myocardial infarction and unstable angina. Myocardial infarction results from an acute total occlusion of the artery, while unstable angina is secondary in most cases to mural thrombus formation. Thrombus formation has also been implicated in chronic atherosclerotic disease progression and in restenosis following coronary angioplasty. Therapeutic measures to treat thrombus rely on the ability of drugs to either prevent thrombus extension, dissolve its fibrin component, or prevent further platelet aggregation. Other measures rely on the ability of intracoronary techniques to open coronary arteries. The primary prevention of intracoronary thrombus formation is evolving. Measures to stabilize plaques or to reduce hypercoagulability are being tested or have been tested in recent trials.     

Stenting for ischemic heart disease

This article examines current indications to intracoronary stenting for percutaneous cardiac revascularization. The data sources are a review of the published English literature, with focus on clinical and randomized trails of coronary artery stenting. Stents reduce the need for emergency bypass surgery in the setting of acute or threatened vessel closure after percutaneous transluminal coronary angioplasty (PTCA). In selected cases, when deployed electively in large native vessels with focal stenosis, clinical and angiographic recurrence are significantly reduced. Preliminary studies have also suggested a potential role in the treatment of saphenous vein graft lesions and restenotic lesions, and in improving on suboptimal results in lesions refractory to balloon dilatation. To prevent stent thrombosis, adjunctive antiplatelet therapy has been shown to be more efficacious than anticoagulation, and optimal stent apposition to the vessel wall appears to be critical. A recent exponential increase in the use of coronary stents has revolutionized the contemporary practice of interventional cardiology. Although technical factors and feasibility have been well refined and shown, evidence-based practice is lacking for many patient subsets.     

Changes in hemostasis in ischemic heart disease

The relationship between changes in blood coagulation, the occurrence and severity of risk factors of ischemic heart disease and the clinical condition of the patient was investigated. The at risk group of patients 42.2% had more than 3 pathological parameters. Intravascular blood coagulation was not activated in any of the patients. In patients with acute myocardial infarction (MI), 62.2% had more than 3 pathological parameters on the first day of MI development. Demonstrable activation of intravascular blood coagulation was found in 28.2% of these patients. On day 5 of MI, activation of intravascular blood coagulation was recorded in 57.7% of the patients treated by classical approach and in 15.4-30.8% of the patients on thrombolytic treatment. In the at risk group, primary hemostasis and the fibrinolytic system were more affected, in patients with MI the whole hemostatic mechanism was involved. On day 5 of MI, in patients with classical therapy pathological laboratory findings still persisted or were even more deteriorated, particularly increases in fibrinogen level. At that time, in patients on thrombolytic therapy no substantial changes of initial values were recorded. No correlation was found to exist between changes in hemostasis and the risk profile or between changes in hemostasis and the clinical severity of MI. The obtained results justify the administration of antithrombotic substances, especially in patients with unstable angina pectoris. On observing time constraints, administration of thrombolytics is justified in MI. (Fig. 9, Ref. 25.)     

Retrograde blood circulation and ischemic heart disease

The author performed experiments on 350 dogs and X-ray postmortem studies of 1520 corpses of subjects who had died of various diseases and injuries. It was found that in occlusive great vessels in the ischemic organs and tissues, retrograde circulation developed, which completely maintained their viability under definite conditions. Retrograde venous blood flow to diseased organs and tissues drastically increased in insufficient retrograde arterial blood circulation. Under certain conditions, surplus venous blood influx caused edema and their dysfunctions. The mechanisms of retrograde circulation account for asymptomatic occlusion of the great vessels.     

Ergometry and the risk factors in ischemic heart disease

The correlational connection between some factors of risk and ergometric indices in patients with ischemic heart disease was studied. The results of an examination covering 188 patients and 56 practically healthy persons which involved the use of a graded stepwise increasing loading on a veloergometer under a monitored control of the pulse rate, ECG and arterial pressure were analyzed. To the risk factors were referred hypercholesterinemia, hypertension, smoking, obesity and hypodynamia. With a rising number of risk factors a significant and progressive decline of the patients' physical performance capacity was ascertained. The most essential correlational connection between the risk factors and the maximally tolerable load and chronotropic and aerobic reserves was educed.     

Cardiopulmonary diagnosis in patients with ischemic heart disease

It may be established that the complex cardiopulmonary functional diagnostics in patients with chronic ischaemic heart disease obtained the following essential results: 1. The ergometrically achieved total functional capacity is clearly decreased in all age groups compared with the healthy persons, the differences are highly significant. 2. The proof of a coronary insufficiency got by the electrocardiogram after work is to be regarded as a factor limiting the functional capacity. 3. 72% of the patients reveal under load a PAEDP increased more than the normal of 25 Torr. After exclusion of a respiratory insufficiency these findings must be regarded as a disturbed myocardial function. 4. Thus the increased PAEDP under load apart from the well-known triad (angina pectoris under load, decreased total functional capacity, pathological ECG after work) is a sensitive and decisive factor for proving the disturbed cardial function in chronic ischaemic heart disease.     

Disorders of intraventricular conductivity in ischemic heart disease

An experience of the vascular surgery department with reconstructive interventions on large arteries of patients with malignant tumors of the lower extremities soft tissues, located in the zone of large vessels of the inguinal region, femur and popliteal fossa, is reported. According to the author's opinion, it is necessary to take into account the fact that in reconstructive procedures on large arteries in patients, subjected to massive repeated radiotherapy, there is an increased danger of occurrence of arrosion hemorrhage, extensive thrombosis of vascular grafts and arteries changed under the effect of ionizing radiation.     

Sotahexal pharmacodynamics in patients with ischemic heart disease

Therapeutic and prophylactic antiarrhythmic efficacy of sotalol hydrochloride (Sotahexal, "Hexal", Germany) and its effects in intracardiac hemodynamics and ECG parameters were evaluated in 95 patients with ischemic heart disease (IHD). The highest response to the drug was observed in ventricular extrasystoles, arterial flutter and fibrillation. Acute episodes of arrhythmia are managed by bolus administration of Sotahexal [correction of Hexal]. In this case greater risk of side effects exists. It is desirable to decide on the drug dose, mode of administration on the individual basis with due consideration of the risks and dangers which could be avoided in case of adequate instrumental control.     

Role of noninvasive examinations in the management of ischemic heart disease.IV. Nuclear cardiology in chronic ischemic heart disease

We evaluated the circadian rhythms in the plasma concentrations of cortisol, cortisone and their free forms, and in the cortisone/cortisol ratios by means of reversed-phase high performance liquid chromatography in normal adult subjects. Plasma concentrations of cortisone, as well as cortisol, exhibited a circadian rhythm. The ratios of cortisone/cortisol remained almost constant during the waking hours of normal subjects. Changes in the cortisone/cortisol ratios previously reported in patients with various diseases exceeded the diurnal changes detected in the present study. Thus, the determination of the cortisone/cortisol ratio provides information that is useful in assessing the adrenal function of patients with various diseases.     

Metabolic disarrangement in ischemic heart disease and its therapeutic control

The term myocardial ischaemia describes a condition which exists when fractional uptake of oxygen in the heart is not sufficient to maintain the rate of cellular oxidation. This leads to extremely complex situations which have been extensively studied in recent years. A large amount of experimental research has been directed to establish the precise sequence of biochemical events leading to myocyte necrosis as such knowledge could lead to rational treatments designed to delay myocardial cell death. At the present time there is no simple answer to the question of what determines cell death and no recovery on reperfusion. Problems arise because: (1) ischaemic damage is not homogeneous and many factors may combine to cause cell death; (2) severity of biochemical changes and development of necrosis are usually associated (both processes being dependent on the duration of the ischaemia) and it is impossible to establish a causal relationship; (3) the inevitability of necrosis can only be assessed by reperfusion of the ischaemic myocardium. Restoration of flow, however, might result in numerous further negative consequences, thus directly influencing the degree of recovery. From the clinical point of view, I have recently learned that there are several potential manifestations and outcomes associated with myocardial ischaemia and reperfusion. Without doubt ventricular dysfunction (either systolic or diastolic) of the ischaemic zone is the most reliable clinical sign of ischaemia, since ECG changes and symptoms are often absent. The ischaemia-induced ventricular dysfunction, at least initially, is reversible, as early reperfusion of the myocardium results in restoration of normal metabolism and contraction. In the ischaemic zone, recovery of contraction might occur instantaneously or, more frequently, with a considerable delay, thus yielding the condition recently recognized as the stunned myocardium. On the other hand, when ischaemia is severe and prolonged, cell death might occur. Reperfusion at this stage is associated with the release of intracellular enzymes, disruption of cell membranes, influx of calcium, persistent reduction of contractility, and eventual necrosis of at least a portion of the tissue. This entity has been called reperfusion damage by those who believe that much of the injury is the consequence of events occurring at the moment of reperfusion rather than as result of changes occurring during the period of ischaemia. The existence of reperfusion damage, however, has been questioned, and it has been argued that, with the exception of the induction of arrhythmias, it is difficult to be certain that reperfusion causes further injury. The existence of such an entity has clinical relevance, as it would imply the possibility of improving recovery with specific interventions applied at the time of reperfusion. In 1985 Rahimtoola described another possible out-come of myocardial ischaemia. He demonstrated that late reperfusion (after months or even years) of an ischaemic area showing ventricular wall-motion abnormalities might restore normal metabolism and function. He was the first to introduce the term hibernating myocardium, referring to ischaemic myocardium in which the myocytes remain viable but in which contraction is chronically depressed. Our data on metabolic changes occurring during ischaemia followed by reperfusion obtained either in the isolated and perfused rabbit hearts or in CAD patients undergoing intracoronary thrombolysis or aortocoronary by-pass grafting will be reviewed.     

Psychological factors and depressive symptoms in ischemic heart disease.

The aim of this study was to determine whether learned helplessness, cognitive distortions, self-efficacy, and dispositional optimism assessed at Time 1 (T1; questionnaires mailed at 1 month postdischarge) would predict depressive symptoms at Time 2 (T2; questionnaires mailed at 1-year follow-up) in a sample of 86 patients hospitalized with ischemic heart disease. Multiple regression results indicated that optimism and cognitive distortions at T1 were significantly associated with T1 depressive symptoms after controlling for confounding variables. When the T1 psychological factors were analyzed with T2 depressive symptoms, only optimism continued to predict depressive symptoms after controlling for confounds and T1 depressive symptoms. The global expectancies that optimism assessed appeared to be more stable over time than the statelike beliefs of cognitive distortions and may have accounted for why optimism predicted T2 depressive symptoms. (PsycINFO Database Record (c) 2010 APA, all rights reserved)