Study of Pacemaker and Implantable Cardioverter Defibrillator Triggering by Electronic Article Surveillance Devices (SPICED TEAS)

The magnetic fields emitted by electronic article surveillance (EAS) systems (shoplifting gates) are a source of interference for implanted medical devices. In the Study of Pacemaker and Implantable Cardioverter Defibrillator Triggering by Electronic Article Surveillance Devices (SPICED TEAS), 25 adult volunteers with ICDs and 50 with pacemakers were exposed to the fields of six different EAS systems. These EAS systems used three modes of operation: magnetic audio frequency, swept radiofrequency, and acoustomagnetic technology. No ICD exhibited interference mimicking sensing of tachyarrhythmias with any EAS system. Pacemakers interacted variably, depending on the type of EAS system. Swept radiofrequency systems produced no interaction with any implanted medical device. One magnetic audio frequency system interacted with 2 of 50 pacemakers. The acoustomagnetic system interacted with 48 of 50 pacemakers. Interactions included asynchronous pacing, atrial oversensing (producing "EAS induced tachycardia" in the ventricle), ventricular oversensing (with pacemaker inhibition), and paced beats resulting from the direct induction of current in the pacemaker ("EAS induced pacing"). These interactions produced symptoms in some patients (palpitations, presyncope) only while patients were in the EAS field. No pacemaker was reprogrammed. We conclude that high energy, pulsed low frequency EAS systems such as acoustomagnetic systems interfere with most pacemakers. Pacemaker patients should be advised to minimize exposure to the fields of such systems to prevent the possibility of serious clinical events.

Environmental electromagnetic interference from electronic article surveillance devices: interactions with an ICD.

A patient with an implantable cardioverter defibrillator (ICD) experienced an inappropriate firing while in close proximity to an electronic article surveillance (EAS) device. Testing revealed the ICD was able to detect high frequency "noise" when close to the EAS device. ICD patients may need counseling to avoid close contact with such devices.

Clinical effects and utility of intracoronary diltiazem.

Coronary artery spasm is a known complication of coronary interventions, for which intracoronary nitroglycerin (ICN) is the treatment of choice. Some forms of intense spasm are resistant to ICN. Calcium channel antagonists are also known to be effective for coronary artery spasm, including nitroglycerin-resistant spasm. Here we describe a protocol for the clinical use of intracoronary diltiazem (ICD). By this protocol, ICD can be safely given without disturbing the clinical status of patients. ICD (2.5 mg) given slowly over 1 minute produced no vasodilitation of normal vessel segments but did produce significant dilatation of stenotic segments above and beyond the effects of nitrates. Mean minimum lumen diameter increased 18%, from 0.89 +/- 0.06 mm to 1.06 +/- 0.07 mm (mean +/- SEM, P < 0.001). ICD produced clinically insignificant changes in systolic blood pressure, diastolic blood pressure, heart rate, and PR, QRS, and QT intervals. This protocol has been employed to safely use ICD to relieve both nitroglycerin-resistant epicardial artery spasm and nitroglycerin-resistant distal microvascular spasm (the no-reflow phenomenon).

New techniques for guiding catheter management during directional coronary atherectomy.

Directional coronary atherectomy (DCA) is an important advance in the mechanical revascularization of stenotic coronary arteries. The bulky nature of the DCA device has necessitated the use of guiding catheter designs that are more cumbersome to use than balloon angioplasty guiding catheters. Because engagement of coronary artery ostia with the currently available DCA guiding catheters is often difficult and because DCA guiding catheters significantly "relax" and reshape during the atherectomy procedure, angiography using these guiding catheters before and after atherectomy can be suboptimal. A new technique for angiography during atherectomy using long Judkin's diagnostic catheters inserted through the existing DCA guiding catheters is described. This technique can be used for optimal visualization of the coronary arteries with minimal use of contrast before and after sessions of atherectomy and also can be used to help engage the DCA guiding catheters. Some improvements in the design of guiding catheters for DCA are suggested.

Acute fluoride toxicity. Pathophysiology and management.

Acute intoxication with inorganic fluoride disrupts numerous physiological systems. As a potent acid it acts corrosively on the skin and mucous membranes, producing severe burns. As the most electronegative element it tightly binds many cations essential to homeostasis, producing, for example, profound hypocalcaemia and resultant inhibition of normal blood coagulation. As a metabolic poison it stimulates some enzymes, such as adenylate cyclase, and severely inhibits others, such as Na(+)-K(+)-ATPase and the enzymes of carbohydrate metabolism. Death can result from these processes and also from a delayed, explosive hyperkalaemia. Therapy of acute poisoning is aimed first, at preventing the absorption of fluoride by incorporating it into insoluble fluoride compounds; secondly, at enhancing fluoride tolerance by maintaining normal blood pH and electrolytes, and aggressive general support of the toxic patient; and thirdly, at manipulating renal excretion or removing fluoride with dialysis and haemoperfusion. If the poisoned patient can be supported for 24 hours, the prognosis improves markedly, although delayed toxicity can occur.

Effect of guar gum on mineral balances in NIDDM adults.

The self-selected diet of 16 subjects with non-insulin-dependent diabetes mellitus (NIDDM) was supplemented for 6 mo with either a granolalike bar containing 35.5 g carbohydrate and 6.6 g guar gum/bar or a placebo bar containing carbohydrate but no guar gum. Subjects consumed a mean of 4.8 bars/day. Average guar gum consumption at the end of the study was 31.7 g/day. One week before and at the end of the study, subjects were admitted to a metabolic ward and fed a controlled diet similar to their self-selected diet. Food, feces, and urine were composited for analysis of iron, zinc, copper, calcium, magnesium, and manganese. Eight subjects consuming the guar gum supplement and 6 subjects consuming the placebo bar completed collections for mineral balance. Neither consumption of guar gum nor placebo bar significantly changed apparent mineral balance for iron, copper, zinc, calcium, manganese, or magnesium from prestudy levels to 6-mo levels, and no significant differences were observed between the two groups. With the exception of copper, men consumed significantly more minerals than women. We conclude that consumption of guar gum by patients with NIDDM does not adversely affect apparent mineral balance.

Search and retrieval of a radiolucent foreign object.

Successful percutaneous removal of an intravascular foreign body requires precise localization of the object so that retrieval devices can be properly positioned. Here we report the successful search for and retrieval of a catheter embolus lost in the ascending aorta during PTCA whose localization was complicated because it was radiolucent.

Dissociation of changes in apparent myofibrillar Ca2+ sensitivity and twitch relaxation induced by adrenergic and cholinergic stimulation in isolated ferret cardiac muscle.

In isolated, aequorin-injected ferret cardiac muscle we measured the apparent myofilament Ca2+ sensitivity and its relationship to twitch relaxation time in the presence of autonomic perturbations. The Ca2+-tension relation was determined from the peak aequorin luminescence and peak twitch tension measured in muscles across a broad range of bathing [Ca2+] in the presence and absence of acetylcholine (ACh) (1 microM) or isoproterenol (ISN) (1 microM), or both drugs. ACh shifted the relationship of peak tension to (peak) aequorin light leftward, which suggests an increase in myofilament Ca2+ sensitivity, but it did not alter relaxation, which was measured as the time for peak tension to decay by 50% (t 1/2 R). ISN produced its previously documented effects, i.e., a rightward shift of the relationship of peak tension to peak aequorin light and a decrease in t1/2R. ACh abolished the ISN effect on the peak tension-aequorin light relationship but did not reverse the effect of ISN to decrease t1/2R. The effects of ACh and ISN of modulating the apparent myofilament Ca2+ sensitivity in intact muscles, corroborate findings of previous studies in isolated myofibrillar preparations. However, these perturbations of myofilament Ca2+ sensitivity in the intact muscle do not relate to twitch relaxation, measured as t1/2R, since (a) ACh affects the former but not the later and (b) the effect of ISN on the Ca2+-tension relationship is abolished by ACh, while the relaxant effect persists.

Subclavian-coronary steal through a LIMA-to-LAD bypass graft.

Eighteen months after coronary artery bypass grafting with a left internal mammary artery (LIMA) graft, a 58-year-old woman had a change in the character of her angina to include pain in the left arm, especially with upper extremity work, culminating in an episode of prolonged rest pain. Cardiac catheterization revealed retrograde flow through the LIMA graft to the subclavian artery and stenosis of the left subclavian artery at its origin from the aorta. Restoration of antegrade flow through the LIMA graft to the coronary arteries was achieved by a carotid-subclavian bypass resulting in a resolution of symptoms. The evaluation of recurrent angina after LIMA bypass grafting should exclude the possibility of subclavian artery stenosis as well as disease of the native and graft coronary anatomy.

Fluoride-induced hyperkalemia: the role of Ca2+-dependent K+ channels.

Acute fluoride poisoning is associated with sudden cardiac death by an unknown mechanism. Because F- binds to Ca2+ to cause marked hypocalcemia, lowered serum Ca2+ concentrations have been thought to be a major underlying factor in the ventricular irritability of F(-)-toxic patients. However, correction of the hypocalcemia does not prevent sudden death. Paradoxically, while decreasing extracellular Ca2+ levels, in vitro studies have shown F- increases intracellular Ca2+, which is thought to trigger Ca2+-dependent K+ channels and produce a K+ efflux. The K+ efflux may be important clinically, as patients with F- overdose can exhibit hyperkalemia shortly before cardiovascular collapse. In erythrocyte suspensions, we found that propranolol, which increases the sensitivity of the Ca2+-dependent K+ channels, exacerbates the efflux, and quinidine, which blocks the channel, prevents the efflux. In six dogs, 35 mg/kg of sodium fluoride given intravenously produced intractable ventricular fibrillation within 140 minutes. Four dogs given 200 mg of quinidine sulfate with the sodium fluoride developed no ventricular arrhythmias. The data indicate that F--induced hyperkalemia is important in sudden cardiac death following acute fluoride toxicity and that this hyperkalemia is mediated by Ca2+-dependent K+ channels.

Delayed fatal hyperkalemia in a patient with acute fluoride intoxication.

A 19-year-old man presented with acute fluoride poisoning. Initially his serum electrolytes were normal, but two hours later he developed ECG evidence of hyperkalemia followed by refractory ventricular fibrillation, suggesting that hyperkalemia may be important in the cardiotoxicity of acute fluoride intoxication. Treatment of fluoride-induced hyperkalemia consists of removal of fluoride from the body by dialysis, binding fluoride with aluminum or calcium, or enhancing fluoride excretion by inducing a metabolic alkalosis. Direct treatment of the hyperkalemia with glucose, insulin, and bicarbonate is ineffective. Quinidine may be an effective therapy for the hyperkalemia and ventricular irritability, but is as yet untested in human beings.

Sodium fluoride produces a K+ efflux by increasing intracellular Ca2+ through Na+-Ca2+ exchange.

Acute fluoride intoxication increases intracellular calcium (Cai), manifested by increased twitch tension in cardiac muscle, and by potassium efflux (mediated by Ca2+-dependent K+ channels) in fluoridated erythrocytes. Fluoride, like isoproterenol, stimulates adenylate cyclase, and could increase Cai via the effects of cAMP on Ca2+ channels. However, while the inotropic effects of fluoride mimicked isoproterenol in rat atria, their effects on the time course of isometric contraction were quite different. In addition, acetylcholine negated isoproterenol's effect on twitch tension but did not modulate the effects of fluoride. Further, the Ca2+ channel antagonist verapamil had no effect on fluoride-stimulated K+ efflux from erythrocytes. Fluoride also inhibits Na+-K+ ATPase, and increases intracellular Na+, so could increase Cai via Na+-Ca2+ exchange. Lanthanum, which blocks Na+-Ca2+ exchange, blocks fluoride-induced K+ efflux in erythrocytes. We conclude that the effects of fluoride on adenylate cyclase are not important in intact tissue, and that inhibition of Na+-K+ ATPase and subsequent Na2+-Ca2+ exchange may be the mechanism of increased Cai in acute fluoride toxicity.

Sudden cardiac death from acute fluoride intoxication: the role of potassium.

The mechanism of sudden cardiac death following acute fluoride intoxication has been thought to result from profound hypocalcemia produced by the precipitation of calcium fluoride salts. In studies of a canine model, the onset of lethal ventricular arrhythmias was temporally more associated with an elevation of serum potassium than with a drop in serum calcium. Fluoride-induced hyperkalemia could not be prevented with glucose, insulin, or bicarbonate. In the erythrocytes, a five-minute exposure to 10 mM NaF caused a 50% increase in extracellular potassium concentrations after 12 hours compared to control erythrocyte suspensions (P less than .001). The total potassium efflux after 12 hours of incubation was linearly related to the log of fluoride contact time (r, 0.886; P less than .001). The treatment of fluoride-induced hyperkalemia may depend on removal of fluoride and potassium.

Nausea and vomiting during acute myocardial infarction and its relation to infarct size and location.

Nausea and vomiting occurring during myocardial ischemia is believed to be associated with inferior wall infarction. However, data supporting such an association are limited, and an alternative hypothesis that cardiac vomiting is related to infarct size has also been advanced. The 2 hypotheses were tested in a cross-sectional study of 265 patients consecutively admitted to the coronary care unit. Nausea or vomiting was a good predictor of myocardial infarction (p less than 0.0001). The odds of having an infarction was 3.14 times greater for patients with nausea or vomiting than for those without these symptoms. Nausea was not a good predictor for inferior wall infarction (p = 0.14): 51% of patients with inferior infarcts had nausea or vomiting and 66% with anterior infarcts had these symptoms. Using peak serum creatine kinase level as an index of infarct size, nausea or vomiting was a good predictor of larger infarction. While 55% of all patients with infarction had nausea or vomiting, for patients with infarctions that produced a peak creatine kinase level of more 1,000 IU/liters, 78% had nausea or vomiting. Sex was a marginally important variable. After adjusting for sex, the presence of nausea or vomiting still predicted infarct size (p less than 0.001). Thus, cardiogenic nausea and vomiting are associated with larger myocardial infarctions but do not suggest infarcts in a particular location.

Nutritional risk of high-carbohydrate, guar gum dietary supplementation in non-insulin-dependent diabetes mellitus.

Dietary supplementation with high-carbohydrate, guar gum fiber (HCF) is effective in acutely blunting postprandial blood glucose levels. We report the effect of such supplementation on the diet and nutritional status of a group of 16 subjects with non-insulin-dependent diabetes mellitus (NIDDM) who incorporated either HCF bars (35.7 g carbohydrate and 6.6 g guar gum/bar) or placebo bars (identical except for the absence of guar gum) into the diet for 6 mo as part of a double-blind, randomized clinical trial. The HCF subjects achieved mean daily intake of 4.8 +/- 0.4 bars, constituting 51.2 +/- 3.1% of total calories and providing 29.7 +/- 2.6 g guar gum daily. Energy intakes and body weight did not change significantly in either group. Food consumption patterns and nutrient intakes did change, although not enough to impair the nutritional integrity of the diet because the bars themselves served as a source of nutrients. The bars were rich in thiamin, B6, folacin, phosphorus, iron, zinc, and copper, adequately replacing any decrease in nutrient intake as a result of foods being dropped from the diet. In fact, daily intakes of B6, folacin, and copper actually increased due to contributions from the bars. Nutrients in which the bars were poor (vitamins A, C and B12) resulted in suboptimal intakes (less than 66% RDA). Although no significant change in nutritional status of the HCF group occurred as determined by arm muscle area, arm fat area, hemoglobin, hematocrit, or serum albumin, transferrin, iron, ferritin, calcium, phosphate, B12, and magnesium levels, these indicators of nutritional status are rather insensitive.(ABSTRACT TRUNCATED AT 250 WORDS)

Long-term effects of guar gum on blood lipids.

While guar gum has been shown to lower total cholesterol and low density lipoprotein cholesterol (LDL-C) in diabetic patients over the short-term, the long-term effects are less well studied and may be unpredictable. Granola bars with and without 6.6 g guar gum were developed and fed to 16 adult volunteers with Type II diabetes mellitus who had been randomized in a double-blind fashion into guar and placebo groups of equal size. Four to six bars were consumed daily with an ad lib diet over a 6-month period. Total cholesterol, total high density lipoprotein cholesterol (HDL-C), subfractions HDL2-C and HDL3-C, LDL-C, and beta-apoprotein were measured at 0 and 6 months. Although LDL-C was lower and triglycerides higher at 6 months than at baseline, these changes were of equal magnitude and direction in both guar and placebo groups. Using each subject as his own control, only the change in triglycerides was statistically significant (P less than 0.025). When male subjects alone were analyzed, the guar group showed a statistically significant decrease in LDL, while the placebo group did not. Other lipid parameters were not significantly changed during the study, despite a positive effect on carbohydrate metabolism from the guar bars. The data suggest either that the hypolipemic effects of guar gum in patients with Type II diabetes mellitus are not sustained for 6 months, or the effects occur only in men.

The manipulation of potassium efflux during fluoride intoxication: implications for therapy.

Based on findings in 2 fluoride-toxic patients, it was suspected that hyperkalemia played a clinically important role in the etiology of sudden death from fluoride poisoning. Using fluoridated human erythrocytes as an in vitro model, it was confirmed that fluoride produced a marked potassium efflux from intact cells. Further, neither glucose and insulin in pharmacologic doses, nor various buffers could halt the efflux by shifting the potassium intracellularly. If these results can be extrapolated to the clinical situation, removal of potassium and fluoride via exchange resins or dialysis remains the only reasonable approach to this life threatening problem. Aside from sudden hyperkalemia and hypocalcemia, no serologic marker for fluoride toxicity has been identified. A high degree of clinical suspicion is therefore essential to the diagnosis.

Long-term ingestion of guar gum is not toxic in patients with noninsulin-dependent diabetes mellitus.

The use of diets rich in unabsorbable carbohydrate ("fiber") has been advocated for the treatment of noninsulin-dependent diabetes mellitus (NIDDM). The soluble viscous fibers such as guar gum are most effective in normalizing carbohydrate intolerance in such patients; particulate fibers such as cellulose have little or no effect. While the latter are known to affect many aspects of nutrition when consumed in great quantity, little is known of the toxicity of guar gum. Eight adults with NIDDM are reported here who consumed at least 30 grams of guar gum for at least 16 weeks without any change in hematologic, hepatic, or renal function. Serologic screening revealed no change in lipid, protein or mineral metabolism, and no change in electrolyte balance. It is concluded that consumption of 30 grams of guar gum per day for prolonged periods is without serious consequences.