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 35,110 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infrared laser therapy (300 Hz) combined with balneotherapy and patients' education is more effective than standard sanatorium rehabilitation in patients with ischemic heart disease associated with diabetes mellitus type 2. 81.8% patients showed good response manifesting in less frequent anginal attacks, episodes of pain and painless ischemia and lower doses of antianginal drugs. Systolic and diastolic arterial pressure lowered by 18 and 10 mm Hg on the average, respectively. Multimodality rehabilitation of IHD patients with type 2 diabetes mellitus improves hemostasis, carbohydrate and lipid metabolism. Coronary circulation response lasted for 24 weeks.
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PMID:[Use of infrared laser therapy in patients with ischemic heart disease associated with diabetes mellitus type 2 in health resort]. 1238 May 22

Silent myocardial ischemia is defined as an ischemic episode without chest pain but with transient ST abnormalities during stress testing or Holter monitoring. With Holter monitoring the prevalence of silent myocardial ischemia in hypertensive patients without coronary artery disease is between 25% and 73%. Simultaneous recording of ambulatory 24-h ECG and 24-h ambulatory blood pressure measurements (ABPM) with the option of additional ST-triggered blood pressure measurement is useful to detect silent ischemia and triggers of silent ischaemia. It is surprising that only a few combined 24-h Holter/ABPM devices are on the market, and in turn only three devices allow additional triggered blood pressure measurements. The paper provides an overview of studies investigating hypertensive patients with Holter monitoring for the detection of ST segment depression indicating myocardial ischaemia. Furthermore, requirements for combined devices allowing simultaneous ambulatory 24-h ECG and ABPM are defined.
Blood Press Monit 2003 Feb
PMID:Simultaneous recording of blood pressure and ST-segment with combined, triggered ambulatory 24-h devices. 1260 36

Heart failure is the term used for a cardiovascular syndrome whose definition lacks uniform criteria. It is associated with a very high mortality rate. Approximately 50% of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT). In severe heart failure, death may also occur due to bradyarrhythmias. Other arrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation, and sustained or non-sustained VT. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations (such as fibrosis) may be prominent. Re-entrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. The treatment of the underlying disease process and optimal management of heart failure is of major importance. Revascularization, beta-blocker therapy, and angiotensin converting enzyme inhibitors are all essential to appropriate therapy. Treatment of arrhythmias is performed either because patients are symptomatic or to reduce the risk of sudden cardiac death. The implantable cardioverter-defibrillator (ICD) is the best available therapy to prevent sudden cardiac death from VT. Devices with back-up pacing also offer protection against bradyarrhythmias. There is evidence that patients with sustained VT or a history of resuscitation have the best outcome with ICD therapy regardless of the degree of heart failure. Many of these patients require additional antiarrhythmic therapy (e.g. amiodarone) because of atrial fibrillation or non-sustained VT that may activate the device.
Heart Fail Monit 2002
PMID:Antiarrhythmic therapy in heart failure. 1263 85

It is widely, but mistakenly, believed that ischemic heart disease (IsHD) and its complications are the sole and direct result of reduced coronary blood flow by obstructive coronary artery disease (CAD). However, cardiac angina, acute myocardial infarction (AMI), and sudden cardiac death (SCD) occur in 15%-20% of patients with anatomically unobstructed and grossly normal coronaries. Moreover, severe obstructive coronary disease often occurs without associated pathologic myocardiopathy or prior symptoms, ie, unexpected sudden death, silent myocardial infarction, or the insidious appearance of congestive heart failure (CHF). The fact that catecholamines explosively augment oxidative metabolism much more than cardiac work is generally underappreciated. Thus, adrenergic actions alone are likely to be more prone to cause cardiac ischemia than reduced coronary blood flow per se. The autonomic etiology of IsHD raises contradictions to the traditional concept of anatomically obstructive CAD as the lone cause of cardiac ischemia and AMI. Actually, all the signs and symptoms of IsHD reflect autonomic nervous system imbalance, particularly adrenergic hyperactivity, which may by itself cause ischemia as in rest angina. Adrenergic activity causing ischemia signals cardiac pain to pain centers via sympathetic efferent pathways and tend to induce arrhythmogenic and necrotizing ischemic actions on the cardiovascular system. This may result in ischemia induced metabolic myocardiopathy not unlike that caused by anatomic or spasmogenic coronary obstruction. The clinical study and review presented herein suggest that adrenergic hyperactivity alone without CAD can be a primary cause of IsHD. Thus, adrenergic heart disease (AdHD), or actually adrenergic cardiovascular heart disease (ACVHD), appears to be a distinct entity, most commonly but not necessarily occurring in parallel with CAD. CAD certainly contributes to vulnerability as well as the progression of IsHD. This vicious cycle, which explains the frequent parallel occurrence of arteriosclerosis and IHD, an association that appears to be linked by the same cause, comprises a common vulnerability to deleterious adrenergic actions on the myocardium, lipid metabolism, and vascular system alike, rather than viewing CAD and IsHD as having a putative cause and effect relationship as commonly thought. Adrenergic actions can also cause the abnormal lipid metabolism that is associated with CAD and IsHD by catecholamine-induced metabolic actions on lipid mobilization by activation of phospholipases. This may also be part of toxic catecholamine hypermetabolic actions by enhancing deleterious cholesterol and lipid actions in damaging coronary vessels by plaque formation as well as inducing obstructive coronary spasm and platelet aggregation. This may also cause direct toxic necrosis on the myocardium as well as atherosclerosis in blood vessels. In fact, drugs that inhibit adrenergic actions like propranolol, reserpine, and guanethidine all inhibit arteriosclerosis induced by hypercholesterolemia in experimental animals and prevent carotid vascular disease (associated with stroke) in humans. The concomitant development of myocardiopathy and coronary vascular lesions or coronary and carotid artery intimal medial thickening by catecholamine toxicity is reflected by the frequent primary presentation of patients with catecholamine-secreting pheochromocytoma with cardiovascular disease, ie, hypertension arrhythmias, AMI, SCD, CHF, and vascular disease, which represents a clear example of the primary deleterious impact of catecholamines on the entire cardiovascular system causing adrenergic cardiovascular disease. Thus, like myocardiopathy, CAD and atherosclerosis in general may be the consequences of or a complication of catecholamine actions rather than its putative cause. This report shows how prophylactic bretylium not only prevents arrhythmias but prevents myocardial necrosis, shock, CHF, maintains or restores normal contractility, and lowers mortality in AMI patients by inducing adrenergic blockade.
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PMID:Prevention of ventricular fibrillation, acute myocardial infarction (myocardial necrosis), heart failure, and mortality by bretylium: is ischemic heart disease primarily adrenergic cardiovascular disease? 1535 32

Although the pathogenesis of fissure is not fully understood, we do know that surgical and/or pharmacological sphincterotomy promotes the healing of chronic anal fissures. A number of studies support the hypothesis that local ischemia is the reason for failure to heal in anal fissure. Therefore, sphincterotomy may work because it decreases anal canal resting pressure and enhances microcirculation at the fissure site. The vasomotor tone of arterioles controlled by metabolic and endothelial factors determines perfusion of tissue and fissure healing. In a novel approach, this paper proposes mechanisms for nitric oxide synthesis, regulation and action in the internal anal sphincter. The design demonstrates the direct interdependence between the activity mechanisms of botulinum toxin and nitric oxide. Endothelial lining can modulate not only vascular tone but also internal anal sphincter (IAS) tone. The application of botulinum toxin likely releases the blockage in glyceryl trinitrate bioactivation in smooth muscle cells and suppresses basal continuous sympathetic activity, causing IAS relaxation. Sufficient distension of the IAS during defecation also reduces the risk of trauma during defecation and complication after the trauma. Both eruption of tissue in the fissure region and release of contraction vessel mediators tend to arrest fissure healing.
Med Sci Monit 2005 Feb
PMID:Relation between botulinum toxin and nitric oxide donors in the treatment of chronic anal fissure. 1566 39

Acute renal failure (ARF) is an abrupt decline of renal function, and acute tubular necrosis (ATN) is its more frequent expression. Recent contributions in physiopathological knowledge, specially in post-ischemic ARF, are scarcelly reflected in therapy. Morbidity and mortality due to ARF are very high, mainly in critically ill patients. Prevention and treatment of ATN are based in avoiding nephrotoxicity and renal ischemia. An adequate evaluation of renal risk factors in hospitalized patients is important. Maintaining euvolemia, effective cardiac output and adequate renal perfussion pressure are three paramount factors in ischemia prevention. The best dialytic schedule is not universally accepted. ARF replacement therapy must be flexible, tailoring techniques (IHD, SLED, CRRT) to the clinical situation of patients. There is not a consensus in dialysis dose in ARF. Nevertheless, despite a robust scientific evidence is lacking, some data suggest that a delivered minimum dose of sKtV >1 in IHD or >35 ml/kg/h in CRRT would be beneficial for patient survival.
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PMID:[Common places on clinical management of acute renal failure]. 1605 Mar 94

The liver is continuously exposed to a large antigenic load that includes pathogens, toxins, tumor cells and dietary antigens. Amongst the hepatitis viruses, only hepatitis B virus (HBV) and hepatitis C virus (HCV) cause chronic hepatitis, which can progress to cirrhosis and hepatocellular carcinoma. Of the different antiviral defense systems employed by the tissue, apoptosis significantly contributes to the prevention of viral replication, dissemination, and persistence. Loss of tolerance to the liver autoantigens may result in autoimmune hepatitis (AIH). This review outlines the recent findings that highlight the role and mechanisms of apoptotic processes in the course of liver diseases. Among factors that contribute to liver pathology, we discuss the role of tumor necrosis factor (TNF)-alpha, HBx, ds-PKR, TRAIL, FasL, and IL-1alpha. Since TNF and FasL-induced hepatocyte apoptosis is implicated in a wide range of liver diseases, including viral hepatitis, alcoholic hepatitis, ischemia/reperfusion liver injury, and fulminant hepatic failure, these items will be discussed in greater detail in this review. We also highlight some recent discoveries that pave the way for the development of new therapeutic strategies by protecting hepatocytes (for example by employing Bcl-2, Bcl-XL or A1/Bfl-1, IAPs, or synthetic caspase inhibitors), or by the induction of apoptosis in stellate cells. The assessment of the severity of liver disease, as well as monitoring of patients with chronic liver disease, remains a major challenge in clinical hepatology practice. Therefore, a separate chapter is devoted to a novel cytochrome c-based method useful for the diagnosis and monitoring of fulminant hepatitis.
Med Sci Monit 2005 Nov
PMID:Apoptosis in liver diseases--detection and therapeutic applications. 1625 9

In newborn infants, allopurinol is being tested as a free radical scavenger to prevent brain damage caused by reperfusion and oxygenation after perinatal hypoxia and ischemia (birth asphyxia). To develop rational dosing schemes for future studies, knowledge of the pharmacokinetics in this patient group is essential. In the present study, a population pharmacokinetic model was designed and validated for allopurinol in this specific patient group. One-compartment and 2-compartment models were fitted to plasma concentration time data of 24 newborns entered in 2 clinical trials using nonlinear mixed effects modeling. A bootstrap procedure was performed to check the robustness of the model. The data were best described using a 1-compartment model with linear elimination. Estimated pharmacokinetic parameters were volume of the central compartment (V, 0.79 L/kg) and total body clearance (CL, 0.078 L/h/kg), with 42% and 60% interindividual variability, respectively. The median values for these parameters of 1000 bootstrap replicates were very similar (95% confidence intervals were 0.67 to 0.96 and 0.054 to 0.10 for V and CL, respectively), indicating the robustness of the model. A population pharmacokinetic model has been designed and validated which adequately describes the data of 2 clinical studies in critically ill newborn infants. The model will be used to design dosing strategies for future evaluation of the benefits of allopurinol in these patients.
Ther Drug Monit 2006 Jun
PMID:Population pharmacokinetics of allopurinol in full-term neonates with perinatal asphyxia. 1677 17

The successive pathophysiological mechanisms that develop in the interstitium of tissues when these undergo acute post-traumatic inflammation are considered increasingly complex trophic functional systems for using oxygen. The nervous or immediate functional system presents ischemia-revascularization and edema, which favor nutrition by diffusion through injured tissue. In this phase of the inflammatory response, while the progression of the interstitial edema produces progressive distancing of the epithelial cells from the capillaries, it simultaneously enhances lymphatic circulation, which assumes an unusually important role. During immune system function, tissue nutrition is carried out by leukocytes through symbiosis with bacteria. Improper use of oxygen persists in this immune phase. Activated phagocytes would require anaerobic glycolysis as the main source of ATP for their functions. During this immune phase, lymphatic circulation still plays a major role. The dilatation of lymphatics may be mediated by cytokines, leuokotrienes, and prostaglandins produced at the trauma site by activated resident and infiltrating cells. Finally, the endocrine functional system facilitates the arrival of oxygen, transported by red blood cells and capillaries. Their trophic potential permits the tissue specialization required for tissue repair to take place. However, if complications occur during the evolution of acute inflammation, the tissues could go back to using more primitive trophic mechanisms. In summary, the ability of the interstitial tissue to express increasingly complex nutritional systems in relation to oxygen use could reflect the importance of this space as a battleground for inflammation and, as a result, for evolution.
Med Sci Monit 2006 Oct
PMID:The inflammatory response: an efficient way of life. 1700 15

Dynamics of fatty acid binding protein (FABP) and pro-brain natriuretic peptide (pro-BNP) levels was studied in patients with ischemic heart disease at rest, during transitory myocardial ischemia, and before and after balloon angioplasty. Forty patients were included: 25 patients with stable angina comprised the study group and 15 patients with acute myocardial infarction (AMI) comprised control group. No significant elevation of FABP was revealed after myocardial revascularization, a tendency was noted to elevation of FABP after transitory ischemia. At the background of stress test pro-BNP level significantly rose. Comparison of FABP levels during first 24 hours of AMI and in patients with IHD both at rest and after veloergometry showed that FABP level in AMI was significantly higher. On day 21 of AMI FABP level became lower and did not differ significantly from this parameter in patients with IHD. Data of this work confirm that search of markers of myocardial ischemia in peripheral blood of patients with IHD is justified, and investigation of their role can allow not only to elevate diagnostic value of stress test, but to assess prognosis and to supplement algorithm of examination of patients with suspected IHD.
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PMID:[Dynamics of Fatty Acid binding protein and pro-brain natriuretic Peptide levels in patients with ischemic heart disease at the background of stress test and balloon coronary angioplasty.]. 1731 Sep 60


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