Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High-grade ventricular arrhythmias are common in congestive heart failure (CHF). However, antiarrhythmic drug therapy is indicated only for patients with symptomatic or hemodynamically significant sustained arrhythmias. Before such therapy is initiated, reversible causes of arrhythmias (eg, electrolyte imbalance, drug interactions and toxicity, decompensation of CHF, ongoing ischemia) should be sought out and corrected. Patients with poor ventricular function or a history of CHF should be hospitalized and monitored continuously during initiation and evaluation of antiarrhythmic therapy so that early detection of proarrhythmic response is possible. Therapy should be initiated with the smallest effective dose, which then is increased slowly to minimize the risk of side effects. Drug selection should be guided electrophysiologically or noninvasively, and empirical antiarrhythmic drug therapy must be avoided.
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PMID:Antiarrhythmic drug therapy in congestive heart failure. Indications and complications. 174 42

Nicardipine i.v. bolus (5 mg/5 min) was administered in the pulmonary artery trunk in 13 patients (2 f, 11 m), mean age 48 +/- 8 yrs, affected by ischemia congestive heart failure, with pulmonary hypertension (pulmonary vascular resistances greater than 6 U.W. and/or systolic pulmonary artery blood pressure greater than or equal to 60 mmHg). The vasodilatation induced by nicardipine caused a rapid improvement of all hemodynamic parameters, with a significant reduction of systemic and pulmonary pressures and resistances; in addition, cardiac output increased significantly. Even if heart rate decreased and mean right atrial pressure fell, their variation did not reach statistical significance. These beneficial effects are attributable to the vasodilator action of nicardipine on the systemic and pulmonary vascular districts. Therefore, in the hemodynamic evaluation of patients with ischemic cardiomyopathy proposed for heart transplantation, we propose the employment of nicardipine in testing the vascular reactivity in cases with secondary pulmonary hypertension.
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PMID:[Bolus nicardipine in the hemodynamic assessment for heart transplantation of patients with severe failure of ischemic origin and high pulmonary resistance]. 180 48

This investigation was designed to determine if acute ischemic cardiac injury causes the release of the 98 amino acid (aa) N-terminus of the 126 aa atrial natriuretic factor prohormone (pro ANF). Seventeen patients with acute myocardial infarction, but without clinical evidence of congestive heart failure, had their circulating concentrations of the whole N-terminus (ie, pro ANF 1-98), the midportion of the N-terminus of the ANF prohormone (consisting of aa 31-67; pro ANF 31-67) and creatine phosphokinase (CPK) monitored daily for 14 days. All seventeen patients had elevated plasma pro ANF 1-98 and pro ANF 31-67 concentrations at the time of presentation. Maximal increase on day three post-infarction correlated with the size of infarction estimated by the maximal CPK (r = 0.675; p less than 0.05) but did not correlate with the amount of left ventricular dysfunction. Another three patients with acute myocardial infarction were treated with tissue plasminogen activator (tPA). The measured pro ANF 1-98 and pro ANF 31-67 levels in these patients were within our normal range and significantly lower (p less than 0.001) than seen in patients with acute myocardial infarction not given thrombolytic therapy. Six patients with unstable angina, likewise, had normal circulating pro ANFs 1-98 and 31-67 concentrations during prolonged episodes of chest pain. These data suggest that myocardial necrosis but not ischemia triggers the release of the entire 126 aa prohormone.
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PMID:Acute and sustained release of the atrial natriuretic factor prohormone N-terminus with acute myocardial infarction. 182 42

Experimental studies were conducted into 170 adult male Wistar rats for the purpose of analysis of cellular adaptation processes of the myocardium to acute ischemia. One group of the animals were exposed to physical endurance training, i.e. 180 h of swimming exercises, up to 3 h daily. Positive verification of cardiac hypertrophy was considered a measure of accomplished cellular adaptation. Training-induced increase of relative and absolute heart weight was 25 and 30%, respectively. Acute myocardial ischemia had been produced by ligature of the left coronary artery. There were no significant differences between trained and untrained animals for incidence and size of infarction and postoperative lethality, while cardiac decompensation was less often recorded from trained animals. To study cellular adaptation as well as differences between trained and untrained animals, tissue samples were taken from the non-ischemic part of the left ventricle and checked by means of histology, electron microscopy, morphometry, quantitative histochemistry, and histo-autoradiography 1, 2, 4, 7, and 14 days after occlusion of the coronary artery. The studies have shown endurance training to result in unambiguous modification of structural as well as functional response of the nonischemic heart. Included in such structural modification at cellular level are significant changes in mitochondrial membranes, sarcoplasmic reticulum, and T-system. Structural modification was reflected in changes to the oxidative enzymes and DNA metabolism. Different patterns of cellular reaction could be positively verified up to 14 days after myocardial infarction.
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PMID:Morphometric, histochemical and autoradiographic studies on myocardial cells in experimental cardiac hypertrophy and ischemia. 182 34

Our knowledge and understanding of the structure, mechanism of action and regulation of receptor-adenylate cyclase systems have increased dramatically in the last few years. A family of receptors (including the beta-adrenergic receptors) and guanine nucleotide regulatory proteins (G proteins) have been purified and cloned. Structure-function studies are beginning to provide insight into how the various components of the transmembrane signaling apparatus interact to promote alterations in the activity of the effector systems. Much effort has been devoted to understanding how various pathophysiologic conditions, such as ischemia or congestive heart failure, and the therapeutic methods used to treat such conditions perturb or regulate receptor systems. It has become abundantly clear that such regulation does occur but is not restricted to simple alterations in receptor number, and may well involve covalent modification (phosphorylation) of receptors or alteration in the ability of receptors to interact with G proteins. In addition, regulation of the quantity or functionality of the various G proteins and the catalytic unit of adenylate cyclase itself appear to occur. For example, recent evidence suggests that congestive heart failure in humans is associated with a decreased number of beta-adrenergic receptors as well as an increased quantity of the inhibitory G protein (Gi). These alterations may provide important insight into how to develop new therapeutic methods. Mechanisms generally responsible for transmembrane signaling, how the components are regulated by pathophysiologic conditions, and drugs used to treat disease states are discussed in detail.
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PMID:Adrenergic receptor responsiveness and congestive heart failure. 185 May 73

During an 18-month period 33 patients in whom there were contraindications to the use of iodinated contrast arteriography underwent 40 carbon dioxide/digital subtraction arteriograms for lower extremity ischemia (19), severe hypertension and renal insufficiency (12), or arterial aneurysm (2). Contraindications to iodinated contrast agents included renal insufficiency, congestive heart failure, and contrast hypersensitivity. Sixteen aortic, 15 iliac-femoral-popliteal-tibial, five aorta-iliac-femoral and four aorta-iliac-femoral-popliteal-tibial carbon dioxide/digital subtraction arteriography studies were performed. In 11 studies, imaging of selected arterial segments required the addition of 10 to 60 ml of dilute nonionic contrast. Guided by carbon dioxide/digital subtraction arteriography studies four femoral-tibial bypasses, three aneurysmorrhaphies, two aortorenal bypasses, one aortofemoral bypass and one femoral-femoral bypass were successfully performed in 11 patients. In addition, carbon dioxide/digital subtraction arteriography directed angioplasties of the common iliac (4), superficial femoral (6), popliteal (3), or tibioperoneal trunk (1) were performed in 10 patients. Complications of carbon dioxide/digital subtraction arteriography included transient deterioration in renal function in three patients in whom 20 ml of nonionic contrast was used, a nonfatal myocardial infarction after a popliteal percutaneous transluminal angioplasty in one patient, and transient tachypnea and tachycardia during a carbon dioxide/digital subtraction arteriography study in one patient. Diagnostic arteriograms are obtainable using carbon dioxide as the contrast agent. Carbon dioxide/digital subtraction arteriography permits patients with symptomatic arterial disease at high risk for contrast related complications to safely undergo arteriography and subsequent arterial reconstruction or endovascular intervention.
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PMID:Clinical applications of carbon dioxide/digital subtraction arteriography. 189 74

The endothelium is increasingly recognized as a modulator of vascular tone, and evidence also is accumulating for an important role of the endothelium in humans in vivo. Endothelial release of prostacylin appears to regulate hyperemic blood flow after ischemia and muscle exercise, and the potent vasodilating properties of endothelium-derived relaxing factor (EDRF) are well established. Tonic release of EDRF plays an important role in the regulation of vascular tone in normal subjects, and a reduction of EDRF release in response to muscarinergic stimulation has been described in subjects with uncomplicated hypertension and also in hyperlipidemic patients. These observations point toward an early disturbance of endothelial function in disorders known as risk factors for the development of atherosclerosis. Furthermore, altered EDRF release and responsiveness to stimuli may be involved in the disturbed regulation of peripheral vascular tone in congestive heart failure. The physiological role of the vasoconstricting peptide endothelin-1 is not yet defined, but the study of the vascular actions of the peptide in humans has shown a vasodilating effect (for low dosages or when the vasconstricting effects are blocked), as well as a marked and long-lasting vasoconstricting effect. Although the mechanisms leading to vasodilation are not clear in humans, endothelin-1-induced vasoconstriction appears to be completely dependent on the activity of voltage-operated calcium channels and can be blocked by organic calcium antagonists but not by nitrovasodilators or EDRF. Further clarification of the role of the endothelium will provide a better understanding of circulatory physiology and pathophysiology and eventually may lead to the development of new therapeutic modalities.
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PMID:Endothelial function in humans. Studies of forearm resistance vessels. 191 1

Clinical implications of diffuse slow washout of thallium-201 (DSWO) in exercise-redistribution myocardial SPECT were studied. Thallium-201 washout rate was calculated by Bull's-eye method. DSWO was defined as having abnormal thallium-201 washout rate (less than 30% per 3 hours) in more than two thirds of each coronary artery (CA) area. OF 974 patients whose exercise heart rate exceeded 120/min, 51 (5.2%) showed DSWO and coronary angiography was performed in 43. Twenty-three patients (53%) showed triple vessel disease (3VD), 8 (19%) showed single or double vessel disease (1VD/2VD) and 12 (28%) showed normal CA. Patients with normal CA consisted of 6 patients with hypertrophic cardiomyopathy (HCM), 5 with hypertension (HT) and one with electrocardiographic abnormality only. The causes of DSWO were assessed from the history of effort angina (EA) and congestive heart failure (CHF), delayed fill-in of the perfusion defect and the ratio of lung to heart thallium-201 activity (L/M) at exercise as an indicator of the left ventricular (LV) function. High prevalence of EA (74%), high incidence of scintigraphic delayed fill-in (83%) and normal L/M suggested diffuse LV ischemia as the cause of DSWO in 3VD. On the other hand in patients with 1VD/2VD, LV dysfunction at exercise was considered as the cause of DSWO because of low prevalence of EA (13%) and scintigraphic delayed fill-in (13%) (p less than 0.01, p less than 0.005 each vs 3VD), and high L/M (p less than 0.001 vs 3VD) and high prevalence of CHF (38%, NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical implications of diffuse slow washout of thallium-201 in exercise stress myocardial SPECT]. 192 Sep 45

Coronary artery fistula is an uncommon clinical entity. The most common coronary artery fistula is from the right coronary artery to the right side of the heart, and it is less frequent to the pulmonary artery. The effect of a coronary artery fistula may be physiologically significant because of the steal phenomenon resulting in coronary ischemia. Based on published reports, it is recommended that patients with congenital coronary artery fistulas be considered candidates for elective surgical correction to prevent complications including development of congestive heart failure, angina, subacute bacterial endocarditis, myocardial infarction, and coronary aneurysm formation with rupture or embolization. A patient is presented in whom treadmill-exercise thallium imaging was effective in determining the degree of coronary steal from a coronary artery fistula, leading to successful corrective surgery.
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PMID:Physiologic assessment of coronary artery fistula. 199 55

The diagnostic yield of endomyocardial biopsies in patients with chronic congestive heart failure of non-ischaemic aetiology remains questionable and, therefore, the use of endomyocardial biopsies under such circumstances is at stake. The present report documents the correlation between the histologic interpretation of endomyocardial biopsies and the corresponding cardiac explants in 13 patients who underwent cardiac transplantation. The biopsy diagnoses in these patients varied from 'compatible with dilated cardiomyopathy' (n = 6) to 'non-conclusive' (n = 4), 'ischaemia' (n = 2) and 'borderline myocarditis' (n = 1). Correlation with the corresponding cardiac explants revealed hypertrophy of myocytes as the leading histologic feature in the majority of cases. Because of the non-specific histopathology of dilated cardiomyopathy, the discrepancy between biopsy diagnoses and the leading explant diagnosis is mostly a matter of semantics. Ischaemia was present at high incidence, but is considered a result of imparied myocardial perfusion rather than the prime mechanism of heart failure. In four cardiac explants myocarditis was encountered, while the corresponding biopsies showed no cellular inflammation. In two, the cellular infiltrates suggested an early state of repair. One heart contained an active and extensive lymphocytic myocarditis. The fourth case showed an eosinophilic myocarditis, most likely acquired after the biopsy was taken. These discrepancies almost certainly relate to the sampling error and the time interval between biopsy and onset of symptoms. The immediate diagnostic yield of the biopsy, in this particular subset of patients, was minimal, particularly with respect to the diagnosis 'myocarditis'. Nevertheless, biopsy diagnoses such as 'compatible with' and 'non-conclusive' do contribute to the final categorization and management of these patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic non-ischaemic congestive heart disease and endomyocardial biopsies. Worth the extra? 204 56


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