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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atrioventricular-nodal-conduction abnormalities following cardiac surgery have been attributed to the potassium ion in cardioplegic solutions. To clarify the etiology of these rhythm problems, 15 dogs were subjected to (I) 60 min 4 degrees C potassium cardioplegic arrest; (II) 30 min normothermic ischemic arrest; or (III) cardiac hypothermia without ischemia. In sinus rhythm and during atrial pacing, A-H and H-V intervals, Wenckebach cycle length (WCL), atrial- and AV-nodal refractory periods (ARP and NRP) were measured at 37 degrees C before and 30 min after arrest (groups I and II) and at various myocardial temperatures (group III). Following cardioplegic arrest and reperfusion, all AV-nodal-conduction properties were unchanged from preischemic values. In contrast, unprotected ischemia significantly prolonged AV-nodal-conduction time (P less than 0.01) and myocardial hypothermia resulted in prolonged WCL (P less than 0.01), prolonged functional NRP (P less than 0.05), in addition to delayed A-H interval (P less than 0.05). The data suggest that properties of AV-nodal conduction are preserved following potassium cardioplegic arrest, but impaired by ischemic injury or persistent local cardiac hypothermia.
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PMID:Etiology of atrioventricular-conduction abnormalities following cardiac surgery. 670 Feb 9

Atrioventricular (AV) conduction was studied in isolated, perfused rabbit hearts. Total AV interval was subdivided into the intraatrial, intranodal and His-Purkinje conduction times. Concentrations of Ca, K and Na in the control perfusate were 2.4, 4.5 and 144.8 mM, respectively. Generalized ischemia or hypoxia almost selectively depressed intranodal conduction, engendering a second degree block. Low Ca (0.8 mM) slightly prolonged the intranodal conduction time, whereas high Ca (4.8-7.2 mM) caused a greater prolongation of this interval, often causing intranodal block. High Ca-induced depression of intranodal conduction was antagonized by high K (7.5 mM). Verapamil (0.5-1.0 mg/L) produced a second degree intranodal block. Subsequent elevation of Na concentration to 172 mM (but not high Ca) restored a 1:1 conduction. Tetrodotoxin (2-10 mg/L) did not affect, whereas low Na (108.6 mM) severely depressed intranodal conduction. These results suggest that (1) AV nodal conduction is most vulnerable to reduced oxygen supply, (2) an optimal Ca concentration for AV nodal conduction exists, (3) high K counteracts high Ca-induced depression of AV nodal conduction, and (4) slow Na current may play a major role in generating AV nodal action potentials. Voltage clamp experiments on the AV node substantiated some of these observations.
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PMID:Peculiarities of AV nodal conduction and the role of slow Na current. 721 99

Current management of coronary artery disease has taken a very aggressive approach in which cardiac catheterization plays a prominent role in patient evaluation and in which bypass and angioplasty are commonly used for therapy. The number of cardiac catheterizations and procedures, not surprisingly, have grown in tandem because angiography provides anatomic information that becomes the substrate for justifying interventions. Bypass surgery has been shown to confer a survival benefit compared with medical therapy in patients with multiple-vessel disease and left ventricular dysfunction, but it also is still used in other patient populations with equivocal indications. Comparison studies of percutaneous transluminal coronary angioplasty with medical management have indicated a slight advantage with percutaneous transluminal coronary angioplasty in limiting symptoms, but no evidence yet supports its survival benefit. Angioplasty, however, has become much more common in the last decade, particularly as the initial revascularization technique. Because cardiac catheterization is frequently the nodal branch point between invasive and noninvasive (i.e., medical) management, its application should be limited to high-risk candidates who would receive a survival benefit from these procedures or to those with intractable symptoms. Those who propose that catheterization is the best method for risk stratification argue that noninvasive testing requires physiologically significant disease and that morbid or fatal events can occur with rapid progression of minimal disease. From the studies reviewed, however, the extent of coronary angiographic disease is not clearly predictive of future cardiovascular events. Although some studies found the number of diseased vessels to be independent prognostic variables, most found that it did not add any additional prognostic information beyond that provided from noninvasive testing. Furthermore, there has been an argument that silent ischemia puts patients at higher risk of sudden death or infarction, and these patients need to be catheterized. However, numerous studies have shown that this concern is exaggerated. The studies reviewed found that except for patients with diabetes, those with "silent" or painless exercise-induced ST depression do not have a worse prognosis than those with symptomatic ST depression when cardiovascular death, sudden death, or acute myocardial infarction are considered Clinical and exercise test variables have been underused in estimating prognosis. Specifically, they are rarely used systematically to stratify patients into low-risk groups who do not need catheterization and high-risk groups who should undergo angiography because of possible lesions amenable to bypass or angioplasty.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical and exercise test markers of prognosis in patients with stable coronary artery disease. 781 29

Three patients with carcinoid tumors of the ileum are presented; two had severe intestinal ischemia, one with infarction of the small intestine. In all three cases, histopathological examination revealed elastic vascular sclerosis (EVS) in the mesenteric blood vessels. Intestinal ischemia in the presence of a carcinoid tumor is probably due to a combination of tumoral secretion products, vascular changes, mesenterial retraction and nodal involvement. Selective superior mesenteric artery arteriography is diagnostic. All the reported carcinoid tumors with ischemic manifestations are ileal and invaded the mesentery or had positive nodes or metastases; two-thirds had EVS, and one-third mesenterial vascular luminal narrowing. Intestinal ischemia may be the underlying cause of vague symptoms in patients with a carcinoid tumor. This tumor may be small and must be looked for during laparotomy, mild intestinal ischemia or mesenterial thickening are important signs. Early resection can prevent intestinal complications. An aggressive attitude, including debulking of metastases, is justifiable.
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PMID:Ileal carcinoid tumors and intestinal ischemia. 785 61

A comprehensive review of the literature has revealed that endothelins belong to a family of vasoactive peptides which are formed and released from the endothelium. By producing constriction of the coronary arteries and peripheral blood vessels, endothelins are known both to reduce coronary bloodflow and increase blood pressure and thus can be seen to affect heart function adversely. On the other hand, endothelins are capable of producing positive inotropic and chronotropic effects by directly affecting both the myocardium and nodal tissues. Prolonged actions of high concentrations of endothelins can be seen to induce relative hypoxia in the myocardium which will eventually result in heart dysfunction. The mechanisms of actions of endothelin on smooth muscle cells and cardiomyocytes include interaction with endothelin receptors on the cell surface, activation of phospholipase C through G-proteins, and increase in the intracellular concentration of Ca2+ through the increase in phosphoinositol turnover. Endothelins were found to exert no effects on sarcolemmal Na+,K(+)-ATPase, Na(+)-Ca2+ exchange and Ca2+ pump systems nor on the sarcoplasmic reticular Ca2+ pump system and myofibrillar ATPase activities in the rat heart. Marked elevation in the levels of plasma endothelins and down-regulation of endothelin receptors in ischemia-reperfusion injury, hypertension and chronic diabetes indicate a significant role of endothelins in the genesis of heart dysfunction under different pathological conditions.
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PMID:Role of endothelin in heart function in health and disease. 822 63

Sinus nodes of five symptomatic patients with the long QT syndrome were surgically excised and followed by permanent electronic pacing as part of a new surgical treatment. We examined those sinus nodes by light and electron microscopy with tissue that was promptly fixed at the time of surgery. All five sinus nodes were similarly abnormal. By light microscopy we found distinctive focal fibrosis, some degenerating myocytes and neural elements, and numerous narrowed small vessels. Except in the nerves there was no evidence of inflammation. In electron micrographs the mitochondria within nodal myocytes were abnormally abundant, remarkably pleomorphic, and smaller than those in normal human sinus nodal cells. The ultrastructural features of the degenerated nodal cells were typical of apoptosis, characterized by the absence of inflammation, well-preserved mitochondria, the presence of apoptotic bodies, phagocytosis of these cells by neighboring myocytes, and especially in smooth muscle cells of arterioles, nuclear chromatin margination and nucleolar disintegration. Apoptotic degeneration of nodal myocytes was stochastic, with adjacent cells appearing unaffected. Focal ischemia caused by narrowed vessels may be a contributory factor, and the nerves may harbor some viral infection, but for the nodal myocytes the abnormality appears to be primarily apoptosis, sometimes called programmed cell death. Both the typically episodic clinical features and the terminal event in fatal cases of the long QT syndrome may be due to apoptosis.
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PMID:Apoptosis and pleomorphic micromitochondriosis in the sinus nodes surgically excised from five patients with the long QT syndrome. 840 7

Calcium channel antagonists can reduce calcium overload induced by myocardial ischemia and thereby protect against malignant arrhythmias. However, these drugs may also adversely affect cardiac contractile function. Mibefradil is a new calcium antagonist that can inhibit cardiac calcium current without reducing myocardial force development. The effects of mibefradil on the inducibility of arrhythmias both before and during ischemia were therefore evaluated in animals with healed infarctions. First, a 2-min coronary occlusion was made during the last minute of exercise (n = 48): 25 animals had ventricular fibrillation (susceptible), whereas 23 did not (resistant). On a subsequent day, programmed electrical stimulation (PES, 8 paced beats followed by two extrastimuli) induced ventricular tachycardia in 19 of 25 susceptible animals but in none of the resistant animals (chi square = 24.6, P < .001). Verapamil (n = 14), diltiazem (n = 13) and mibefradil (n = 14) elicited significant dose-dependent decreases in refractory period and in the Q-Tc interval (except mibefradil) yet failed to prevent PES-induced arrhythmias. Diltiazem and verapamil also increased P-R interval and reduced the maximum rate of change of left ventricular pressure, whereas mibefradil did not. However, all three drugs abolished arrhythmias induced by PES during ischemia. In contrast, lidocaine suppressed PES-induced arrhythmias but failed to prevent ischemically induced arrhythmias. Thus mibefradil can prevent ischemically induced ventricular fibrillation without adverse actions on either A-V nodal conduction or contractile function. These data further suggest that calcium entry may play a critical role in the initiation of ventricular fibrillation during ischemia, whereas other factors must be responsible for the extrasystoles induced by PES.
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PMID:The effects of mibefradil, a novel calcium channel antagonist on ventricular arrhythmias induced by myocardial ischemia and programmed electrical stimulation. 866 18

The calcium-channel blockers are an ever-enlarging, heterogeneous group of drugs with widely variable effects on myocardium, sinoatrial and atrioventricular nodal function and conduction, peripheral blood vessels, and coronary circulation. Since the development and characterization of calcium-channel antagonists in the 1960s, these agents have become increasingly important in the treatment of many cardiovascular diseases. Nine calcium-channel blockers-nifedipine, nicardipine, amlodipine, felodipine, isradipine, nimodipine, diltiazem, verapamil, and bepridil-are all approved for use in the United States. Each major category has its own unique physiologic features. These drugs are extremely useful in the management of cardiac arrhythmias (particularly supraventricular arrhythmias) and/or ischemia. As future generations of calcium-channel blockers are developed with greater vasoselectivity, less negative inotropic effects, and reduced tendency to activate the renin-angiotensin system, their indications for use will continue to grow.
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PMID:Antiarrhythmic and anti-ischemic properties of calcium-channel antagonists. 868 75

Arrhythmias occur 24 h after occlusion of the left anterior descending (LAD) coronary artery in the canine heart and have been attributed to the abnormal spontaneous activity in subendocardial Purkinje fibers, which are markedly depolarized. The major current underlying normal automaticity in these fibers is i(f). Although the i(f) activation range is generally considered to be more negative than the diastolic membrane potential in these depolarized fibers in infarcts, this activation range has been shown to shift in a positive direction in response to hormonal influences. Thus i(f) could still mediate automaticity in these fibers in infarcts. Furthermore, recent reports indicate that a depolarizing diastolic current, probably i(f), also can be measured in ventricular muscle during abnormal experimental conditions, which may occur during ischemia. To test whether there is a role of i(f) currents in sustaining ventricular ectopy, we administered the selective i(f) channel blocker, zatebradine, 24 h after LAD ligation in canine hearts. We report that intravenous injections of zatebradine (0.25 or 1.0 mg/kg) significantly slow ventricular rhythms (with average reductions of 19 or 26%, respectively). Moreover, because zatebradine also slows sinus nodal rate, it can lead to an increased incidence of ectopic beats. However, during right atrial pacing, when sinus slowing has no effect on ventricular rhythms, capture of ventricular rhythms occurs at lower rates in the presence of zatebradine. The reduction of capture threshold is comparable to the reduction in the rate of the ectopic rhythm. Thus zatebradine eliminated the arrhythmia when the right atrium was paced at the original sinus rate.
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PMID:Zatebradine slows ectopic ventricular rhythms in canine heart 24 hours after coronary artery ligation. 921 10

Membranous fat necrosis (MFN) is a degenerative process involving mature systemic adipose tissue. It is characterised by the presence of membranocystic foci surrounded by a lipophagic fibro-inflammatory reaction typical of fat necrosis. Membranocystic foci are cysts lined by an eosinophilic membrane with pseudopapillary infoldings having the histochemical staining profile of ceroid. Although MFN is described in an increasing number of adipose tissue sites, it has not been described as a distinct entity in appendices epiploicae (AE). Macroscopically, MFN in AE mimics nodal tuberculosis or metastatic tumour with necrosis and cystic change. Ischaemia, which can be secondary to physiological or pathologic processes, is crucial in the pathogenesis of MFN in AE. Heightened awareness of MFN as a distinct entity in AE is essential for accurate diagnosis and establishment of the pathogenesis of this enigmatic pathological process.
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PMID:Membranous fat necrosis in appendices epiploicae. A clinicopathological study. 953 1


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