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L T Iseri

Publications and source records attributed to L T Iseri.

At least 19 recordsLinked to original sources
PubMed1990

Role of magnesium in cardiac tachyarrhythmias.

The efficacy of magnesium therapy in patients with ventricular tachycardia has previously been reported. Recently completed and ongoing studies validate earlier observations that potassium and magnesium supplementation may control other cardiac arrhythmias, particularly in hypomagnesemic patients. Magnesium treatment is a viable therapeutic option when other antiarrhythmic agents fail to suppress ventricular tachycardia, ventricular fibrillation, multifocal atrial tachycardia, atrial fibrillation and supraventricular tachycardia.

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PubMed1989

Magnesium therapy of cardiac arrhythmias in critical-care medicine.

A common complication of critically ill patients is cardiac tachyarrhythmia. The role played by magnesium is not well appreciated. Well-documented cases indicated that magnesium may be effective in controlling the rhythm when conventional methods fail. The following tachyarrhythmias respond favorably to magnesium: (1) intractable ventricular tachycardia and fibrillation, whether hypo- or normomagnesemic, (2) torsades de pointes, (3) digitalis-toxic ventricular tachyarrhythmia, (4) multifocal atrial tachycardia and (5) hypomagnesemic atrial tachyarrhythmia. It is recommended that 10-15 ml of 20% MgSO4 be infused over 1 min, followed by 500 ml of 2% MgSO4 over 5 h. A second 500 ml over 10 h may be necessary. Renal failure, disappearance of deep tendon reflex, rise in serum Mg above 5 mEq/l, drop in systolic blood pressure below 80 or drop in pulse below 60 contraindicate the continued use of magnesium. If serum potassium is at or falls below 4.0 mEq/l, 20-40 mEq/l KCl should be added. Magnesium deficiency can be confirmed by a low serum level or by a greater than 50% retention of administered magnesium. The causes of magnesium deficiency can be remembered under 10 DS: (1) Diarrhea and gastrointestinal losses, (2) Diuretics and renal losses, (3) Diabetes and endocrine causes, (4) Dietary lack, (5) Diverted to free fatty acids, (6) Drugs such as cisplatin, (7) Drinking alcohol to excess, (8) Delivery with toxemia, (9) Decompensated heart, lungs or liver and (10) Denuded skin, such as burns.

Arrhythmias, Cardiac↗
PubMed1987

Ventricular tachyarrhythmia associated with psychological stress. The role of the sympathetic nervous system.

Psychological stress has been reported to be a risk factor for sudden cardiac death in individuals both with and without underlying structural heart disease. From a group of 80 patients presenting with life-threatening ventricular tachyarrhythmia, six were identified without underlying structural heart disease. Five of these six patients experienced marked psychological stress. Each of these five patients underwent arrhythmia evaluation, demonstrating recurrent rapid monomorphic ventricular tachycardia related to changes in tone of the sympathetic nervous system. Subsequently, solitary beta-adrenergic blocker therapy was given to each patient. During therapy, four of the five patients had a marked reduction of both arrhythmia and symptoms during a follow-up ranging from 29 to 49 (mean, 38) months.

Adrenergic beta-Antagonists↗
PubMed1986

Magnesium and cardiac arrhythmias.

The effectiveness of magnesium therapy in intractable ventricular tachycardia and ventricular fibrillation was documented in patients not only with hypomagnesemia, but also in patients with normomagnesemia. It was also effective in ventricular tachycardia characterized by 'torsades de pointes' and in massive digoxin intoxication. Prospectively, parenteral magnesium therapy was also effective in controlling the ventricular rate in multifocal atrial tachycardia (8 patients) by reducing the number and the rate of ectopic atrial foci. Parenteral magnesium sulfate administration, 10-15 ml of 20% MgSO4 in 1 min and 500 ml of 2% MgSO4 in 5 h in patients without renal failure was found to be safe and effective. Magnesium sulfate prevented hyperpotassemia in massive digoxin intoxication and tended to produce hypopotassemia in other patients necessitating concomitant use of potassium chloride.

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PubMed1985

Magnesium and potassium therapy in multifocal atrial tachycardia.

Eight patients with multifocal atrial tachycardia received 7 to 12 gm of magnesium sulfate intravenously over a 5-hour period. Potassium supplements were given initially or added later. Initial arterial blood gases showed mean pH 7.48 +/- 0.03, PcO2 39.7 torr, PO2 72 torr, HCO-3 29.8 +/- 4.5 mEq/L, and base excess 6.84 +/- 3.78 mEq/L. Initial serum magnesium correlated well with initial serum potassium. Three patients had subnormal levels of magnesium and potassium. The level of serum magnesium rose with an intravenous injection magnesium and serum potassium levels tended to fall unless they were supplanted with potassium. There were seven patients who retained more than 20 mEq of the infused magnesium. Multifocal atrial tachycardia was successfully converted to sinus rhythm or sinus tachycardia in seven patients. Multifocal atrial rhythm (at slow rate) persisted in one patient. Two patients with falling serum potassium levels required potassium supplements. Results of this study confirm that patients with multifocal atrial tachycardia respond favorably to parenteral magnesium and potassium. We believe that serum magnesium administered together with serum potassium stabilizes the ionic balance of atrial cells and thus prevents spontaneous ectopy.

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PubMed1984

Magnesium therapy in massive digoxin intoxication.

A potentially fatal case of massive digitalis intoxication is presented. Recurrent ventricular fibrillation failed to respond to lidocaine or phenytoin, but responded dramatically to magnesium sulfate infusion. A review of the literature and previous clinical studies, as well as the case reported here, appears to indicate that magnesium sulfate given intravenously in adequate quantities (2 to 3 g in one minute followed by 2 g/h for 4 to 5 h) is effective in controlling ventricular irritability caused by toxic levels of digitalis preparations.

Digoxin↗
PubMed1984

Magnesium in coronary artery disease.

Magnesium in coronary artery disease is reviewed with regard to its role in the pathogenesis of arteriosclerosis, coronary spasm, myocardial function, acute myocardial infarction and ventricular arrhythmias. Experimentally, magnesium depletion potentiates and supplementation retards the effect of atherogenic diets. Evidence from human studies is circumstantial. Reactivity of arterial smooth muscle is enhanced by low and suppressed by high magnesium media. Evidence that magnesium depletion may initiate coronary spasm is provided by dog and retrospective human studies. Although experimental magnesium deficiency disrupts myocardial mitochondria, there are no studies which show that magnesium deficiency will lead to cardiac failure or that replacement will improve cardiac function. It is known that an infarcted or ischaemic myocardium loses magnesium and this may be the basis for ventricular arrhythmias. Coronary occlusion in a previously magnesium-depleted heart will result in a larger area of necrosis and ischaemia. The fall in serum magnesium in acute myocardial infarction is probably due to the formation of soap in fat cells undergoing catecholamine lipolysis. Ventricular fibrillation in coronary artery disease will respond to parenteral magnesium, even in the presence of normal serum concentrations.

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PubMed1983

Digital angiography in assessment of ventricular function and wall motion during pacing in patients with coronary artery disease.

Using digital subtraction angiography, left ventriculograms were obtained with 10 ml of iodinated contrast material in 21 patients both at rest and during atrial pacing. In 15 patients with significant coronary artery lesions (CAD) (greater than 50% diameter narrowing in at least 1 major artery), ejection fraction decreased during atrial pacing from a mean of 62 +/- 14% to 51 +/- 15% (p less than 0.001). In 14 (93%) of 15 patients, ejection fraction decreased or was unchanged during pacing. In 6 patients with chest pain but normal coronary arteries, ejection fraction increased from a mean of 66 +/- 9% at rest to 72 +/- 6% during atrial pacing (p less than 0.01). Ejection fraction increased by greater than or equal to 5% during pacing in 5 of 6 patients with normal coronary arteries. Patients with CAD also had an abnormal response in end-systolic volume during atrial pacing (50 +/- 31 ml at rest versus 47 +/- 24 ml during pacing) compared with patients with normal coronary arteries (46 +/- 16 ml at rest versus 26 +/- 9 ml during pacing; p less than 0.01). The digital ventriculograms demonstrated new or increased wall motion abnormalities during atrial pacing in 4 of 5 patients with CAD who had wall motion abnormalities at rest and in 8 of 10 patients with CAD who had normal wall motion at rest. Moreover, these wall motion abnormalities occurred in myocardial wall segments that were supplied by coronary arteries with significant lesions. Thus, because digital subtraction angiography allows multiple left ventriculograms to be obtained during routine cardiac catheterization, intervention studies such as atrial pacing can be used to obtain a functional assessment of the severity of coronary arterial lesions.

Adult↗
PubMed1983

Correlation of 10-milliliter digital subtraction ventriculograms compared with standard cineangiograms.

Left ventriculograms were obtained with the use of 10 ml of contrast media by passing fluoroscopic video images through a video image processor. The low concentration of dye in the left ventricle was enhanced by the technique of mask mode subtraction, and the images were postprocessed to increase visibility by manipulation of the gray scale and contrast levels. These digital subtraction angiograms were compared to standard cineangiograms by means of 40 ml of contrast media. Of 30 patients studied, six (20%) had runs of ventricular tachycardia during the cineangiogram and had to be excluded. In the remaining 24 patients, there was a good correlation between the two techniques for left ventricular end-diastolic volume (r = 0.77, end-systolic volume (r = 0.95), and ejection fraction (r = 0.97). Spatial resolution in the digital studies was adequate to appreciate wall motion abnormalities that were visualized on the cineangiograms. Left ventricular end-diastolic pressure (LVEDP) did not change after the 10 ml injection, but the mean LVEDP rose 6.0 mm Hg after the 40 ml cineangiograms (p less than 0.01). Digital subtraction angiography can be used to obtain left ventriculograms with one-fourth the amount of contrast media and one-fourth the x-ray exposure compared to standard cineangiograms. This technology will permit multiple left ventriculograms to be obtained which, in turn, will allow intervention studies to be performed in the catheterization laboratory.

Adult↗
PubMed1983

Evaluation of dilated cardiomyopathy by pulsed Doppler echocardiography.

The ability of pulsed Doppler echocardiography to identify patients with left ventricular systolic dysfunction was evaluated in 12 patients with dilated (congestive) cardiomyopathy. A range-gated, spectrum analyzer-based Doppler velocimeter was used to record blood flow velocity in the ascending aorta and main pulmonary artery. The following blood flow velocity parameters were measured or derived: peak flow velocity, acceleration time, average acceleration, deceleration time, average deceleration, ejection time, and aortic flow velocity integral. Doppler blood flow velocity data in the cardiomyopathy patients were compared to data from 20 normal subjects. Measurements from the ascending aorta revealed that peak aortic flow velocity discriminated between cardiomyopathy patients (mean 47 cm/sec, range 35 to 62) and normal subjects (mean 92 cm/sec, range 72 to 120) with no overlap in data (p less than 0.001). Aortic flow velocity integral was also able to separate the patients with dilated cardiomyopathy (mean 6.7 cm, range 3.5 to 9.1) from normal subjects (mean 15.7 cm, range 12.6 to 22.5) with no overlap in data (p less than 0.001). Although mean values for average aortic acceleration and aortic ejection time were also significantly different (both p less than 0.005), there was some overlap between the two groups. Pulmonary artery blood flow studies demonstrated significantly increased average acceleration, as well as decreased ejection time (both p less than 0.05), but no difference in average deceleration or peak flow velocity in cardiomyopathy patients compared to normals. Compared to pulmonary flow measurements, aortic Doppler flow velocity measurements allowed better separation of cardiomyopathy and normal groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Magnesium therapy for intractable ventricular tachyarrhythmias in normomagnesemic patients.

Intractable ventricular tachyarrhythmia associated with hypomagnesemia responds well to magnesium given intravenously. Two patients with recurrent ventricular tachycardia and ventricular fibrillation associated with normal serum magnesium levels and resistant to treatment with potassium chloride, lidocaine and bretylium tosylate responded dramatically to the administration of magnesium sulfate. A third patient in whom the serum magnesium level was unknown also showed dramatic response to magnesium therapy. Magnesium depletion probably interferes with sodium-potassium adenosine triphosphatase enzyme activity and causes ionic imbalance and electrical instability of purkinje's fibers. Without obvious magnesium depletion this element in high concentration may still prolong transient inward current, prolong the effective refractory period, increase the membrane potential and control ventricular tachyarrhythmia. When ventricular fibrillation or malignant ventricular tachycardia cannot be controlled with lidocaine and other conventional drugs, we recommend infusing magnesium sulfate, 2 to 3 grams in one minute, followed by 10 grams over five hours.

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