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Biomedical subjects

S Laniado

Publications and source records attributed to S Laniado.

At least 19 recordsLinked to original sources
PubMed1992

Clinical and electrophysiologic effects of magnesium sulfate on paroxysmal supraventricular tachycardia and comparison with adenosine triphosphate.

Electrophysiologic studies have shown that intravenous magnesium sulfate prolongs atrioventricular (AV) nodal conduction and refractoriness and thus could play a role in the management of patients with paroxysmal AV reentrant supraventricular tachycardia (SVT). The present study evaluates the clinical and electrophysiologic effects of intravenous magnesium sulfate in patients with SVT and compares them with those of adenosine triphosphate (ATP), one of the most potent drugs in the treatment of this arrhythmia. Patients with inducible sustained SVT were treated with ATP (10 or 20 mg) and magnesium sulfate (2 g over 15 seconds) during electrophysiologic study. If the tachycardia failed to terminate by the sixth minute, an additional 2 g dose of magnesium was given. ATP (10 or 20 mg) was significantly better than magnesium for terminating induced tachycardias (14 of 14 vs 6 of 14, p less than 0.0001). Arrhythmia termination with ATP was due to anterograde AV nodal blockade in all but 1 patient who developed retrograde block over an accessory pathway with decremental conduction. Arrhythmia termination by magnesium was due to retrograde block over an accessory pathway in 3 patients (including the patient with accessory pathway exhibiting decremental conduction), anterograde AV nodal conduction block in 2 patients and premature ventricular complexes in 1 patient. During induced tachycardias, only AH intervals were prolonged by ATP, whereas magnesium significantly prolonged AH and QRS intervals. Short-lasting side effects (chest pain, flushing, nausea) occurred after both drugs were administered but were more severe after magnesium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1992

Clonidine for patients with rapid atrial fibrillation.

OBJECTIVE: To determine whether clonidine can slow ventricular rate in patients with rapid atrial fibrillation. DESIGN: Randomized, controlled trial, with a 4-hour follow-up period. SETTING: Emergency room of a university hospital. PATIENTS: A consecutive sample of 18 hemodynamically stable patients who were evaluated or treated for rapid atrial fibrillation. Exclusion criteria included acute or terminal illness; current use of antiarrhythmic agents, calcium-channel blockers, or beta-blockers; excessive hypertension; pulmonary, valvular, or pericardial disease; and electrolyte imbalance. INTERVENTIONS: Patients were randomly assigned to receive either "no treatment" (control group) or clonidine, 0.075 mg orally, at baseline and after 2 hours if heart rate did not decrease by at least 20%. MEASUREMENTS: Blood pressure was measured by the same nurse in the same arm for 4 consecutive hours, and a full 12-lead electrocardiographic evaluation was done. MAIN RESULTS: Heart rate decreased to below 100 beats/min in eight of nine patients receiving clonidine compared with two of nine patients in the control group. The difference in the mean decreases in heart rate was 38 beats/min (95% CI, 20 to 56 beats/min). Six patients who were treated with clonidine and one patient in the control group reverted to normal sinus rhythm. Systolic blood pressure decreased slightly in both groups, without significant differences. Clinical follow-up was uneventful. CONCLUSION: Low-dose clonidine was an easy, efficient, and effective treatment for patients with rapid atrial fibrillation who were hemodynamically stable.

Adrenergic alpha-Agonists↗
PubMed1992

Left ventricular filling dynamics by Doppler echocardiography in dilated cardiomyopathy: one-year follow-up in patients treated with captopril compared to placebo.

The role of impaired diastolic function in determining the pathophysiology of congestive cardiomyopathy was only recently appreciated. In the present study, echocardiography and Doppler cardiography were used to determine changes in cardiac size and transmitral filling dynamics over a 1-year period in patients with congestive cardiomyopathy and determine the effect of captopril on these changes. The study population consisted of 27 patients with congestive heart failure in spite of therapy with digitalis and diuretics (NYHA class 3.2). Fifteen patients were started on placebo and 12 on captopril. Noninvasive evaluation was performed at 6-month intervals. Left ventricular size and left ventricular ejection fraction did not change significantly in either group. Forward stroke volume improved significantly only in patients on captopril compared to placebo (p < 0.05). No significant changes in transmitral flow dynamics were observed in the placebo group whereas the captopril-treated group showed a decrease in the peak velocity, flow velocity integral and rate of rapid filling wave (E) and an increase in the peak, integral and rate of filling during atrial contraction (A). The E/A ratio did not change significantly over time in the placebo group, whereas a reduction in the ratio was noted in the captopril-treated patients. These changes are sustained over 1 year with concomitant improvement in stroke volume, exercise duration and functional class.

Aged↗
PubMed1992

Deterioration of ventricular tachycardia to ventricular fibrillation after rapid intravenous administration of magnesium sulfate.

We report the case of a patient who had development of ventricular fibrillation following rapid intravenous administration of magnesium sulfate (2 g over 5 s) for treatment of sustained monomorphic ventricular tachycardia. Initial slowing of the tachycardia was followed by gradual widening of QRS complexes and electrical alternans, leading to ventricular fibrillation within 3 min of magnesium administration.

Aged↗
PubMed1991

Prognostic importance of delayed Q-wave evolution 3 to 24 hours after initiation of thrombolytic therapy for acute myocardial infarction.

The timing of Q-wave evolution and its prognostic significance was studied in 201 patients who received thrombolytic therapy for a first acute myocardial infarction (AMI). One hundred forty-one patients (70%) had evidence of a Q-wave AMI within 3 hours of the initiation of thrombolytic therapy, 31 (16%) developed Q waves after 3 hours but before hospital discharge, and 29 (14%) were discharged with a non-Q-wave AMI. Laboratory indicators of myocardial damage and in-hospital morbidity and mortality were greater among patients with Q-wave AMIs than with non-Q-wave AMIs. When these indexes were examined with respect to the timing of Q-wave evolution, the prognosis of patients with delayed Q-wave development was similar to that of patients with non-Q-wave AMIs. Thus, compared to patients with early (less than or equal to 3 hours) Q-wave evolution, patients with delayed Q-wave evolution or with a non-Q-wave AMI had a smaller creatine kinase peak (mean 661 to 1,081 vs 1,251 to 1,541 IU; p = 0.005), better preservation of left ventricular function as measured by radionuclide ventriculography before discharge (mean +/- standard deviation 54 +/- 11% vs 47 +/- 13%; p less than 0.01), and a lower incidence of congestive heart failure at discharge (3 vs 15%; p = 0.02). In-hospital mortality was lower among patients with delayed Q-wave evolution or with a non-Q-wave AMI (5 of 141 vs 0 of 60; difference not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Incidence of left ventricular thrombi formation after thrombolytic therapy with recombinant tissue plasminogen activator, heparin, and aspirin in patients with acute myocardial infarction.

To evaluate the prevalence of left ventricular thrombi after thrombolytic therapy, 144 consecutive patients with acute myocardial infarction (AMI) were prospectively studied with two-dimensional echocardiography 1 and 8 days after admission. Patients were treated 2.1 +/- 0.8 hours after the onset of symptoms. Thrombolytic protocol included 120 mg of recombinant tissue plasminogen activator (rt-PA), 5000 IU of heparin, followed by a continuous infusion of 25,000 IU/24 hours for at least 5 days, and 250 mg of aspirin a day. Seventy-six patients had AMI of the anterior wall; of these, seven (9.2%) developed left ventricular thrombi. The remaining 68 patients had infarctions of the inferior wall; of these, two (2.9%) developed left ventricular thrombi. Since anterior wall infarction not treated with thrombolytic therapy is associated with a 25% to 40% rate of left ventricular thrombi, we conclude that early thrombolytic therapy with rt-PA, heparin, and aspirin reduces the formation of left ventricular thrombus in AMI of the anterior wall. Apical left ventricular thrombi developed more frequently in patients with previous infarctions compared with those without (4 of 17 versus 4 of 127, p = 0.01). During the 12-month follow-up period, no patient in the study had manifestations of peripheral emboli.

Aged↗
PubMed1991

Atrial contribution to ventricular filling in mitral stenosis.

BACKGROUND: The importance of the contribution of atrial systole to ventricular filling in mitral stenosis is controversial. The cause of reduced cardiac output following the onset of atrial fibrillation may be due to an increased heart rate, a loss of booster pump function, or both. METHODS AND RESULTS: We studied the atrial contribution to filling under a variety of conditions by combining noninvasive studies of patients with computer modeling. Thirty patients in sinus rhythm with mild-to-severe stenosis were studied with two-dimensional and Doppler echocardiography for measurement of mitral flow velocity and mitral valve area (MVA). The mean +/- SD atrial contribution to left ventricular filling volume was 18 +/- 10% and varied inversely with mitral resistance. Patients with mild mitral stenosis (MVA, 1.8 +/- 0.7 cm2) and severe mitral stenosis (MVA, 0.9 +/- 0.2 cm2) had atrial contributions of 29 +/- 4% and 9 +/- 5%, respectively. The pathophysiological mechanisms responsible for these trends were further investigated by the computer model. In modeled severe mitral stenosis, increasing heart rate from 75 to 150 beats/min caused an increase of 5.2 mm Hg in mean left atrial pressure, whereas loss of atrial contraction at a heart rate of 150 beats/min caused only a 1.3 mm Hg increase. CONCLUSIONS: The atrial booster pump contributes less to ventricular filling in mitral stenosis than in the normal heart, and the loss of atrial pump function is less important than the effect of increasing heart rate as the cause of decompensation during atrial fibrillation.

Adult↗
PubMed1990

Programmed ventricular stimulation using up to two extrastimuli and repetition of double extrastimulation for induction of ventricular tachycardia: a new highly sensitive and specific protocol.

The sensitivity and specificity of a new protocol of programmed ventricular stimulation were evaluated in 71 consecutive patients who were divided into 2 groups: group 1 included 41 patients, of whom 25 had sustained ventricular tachycardia (VT) not associated with cardiac arrest and 16 had ventricular fibrillation (VF) not precipitated by any obvious factor; group 2 included 30 patients without demonstrable heart disease and no suspected or documented sustained ventricular tachyarrhythmias. The study consisted of a standard protocol (up to 2 extrastimuli given only once for each extrastimulus prematurity, 2 right ventricular sites and 3 basic pacing cycle lengths, as well as rapid ventricular pacing) in which double extrastimulation at the shortest coupling intervals that allowed ventricular capture was repeated 10 times. A stimulus current of 3 mA was used. Sustained ventricular tachyarrhythmias were induced in 23 of 25 (92%) patients who presented with sustained VT, 14 of 16 (88%) patients who presented with VF and 2 of 30 (7%) group 2 patients. Eighteen of 25 (72%) patients with sustained VT but only 4 of 16 (25%) with VF had arrhythmias inducible at "immediate" trials of single or double extrastimulation (p less than 0.01). Repetition of double extrastimulation increased the yield of inducible sustained ventricular tachyarrhythmia to 92% in patients with sustained VT (+20%, p = 0.14) and 75% (+50%, p = 0.013) in patients with VF. Rapid right ventricular pacing added a 13% increase in the overall yield in patients with VF. This new protocol of programmed ventricular stimulation has both high sensitivity (90%) and specificity (93%) for induction of sustained VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1990

Early thrombolytic therapy does not enhance the recovery of the right ventricle in patients with acute inferior myocardial infarction and predominant right ventricular involvement.

In this study we report the effects of early thrombolytic therapy on the recovery of the right ventricle after an acute myocardial infarction. Sixty-five patients presenting with their first inferior myocardial infarction and predominant right ventricular involvement were consecutively treated as follows: group A (20 patients) conservatively (without thrombolytic therapy), group B (19 patients) with streptokinase and group C (26 patients) with recombinant tissue type plasminogen activator. Coronary angiography was performed within 72 h after admission in 52 patients (10 of group A, 18 of group B and in 24 patients of group C) followed by transluminal coronary angioplasty in 26. All groups had similar characteristics except for a higher mean age in group A. Within 3 months, a remarkable improvement in right ventricular function and a major increase in ejection fraction was observed for all three patient groups. Improvement of right ventricular function was more prominent in patients with residual flow through the infarct-related artery. The beneficial course was comparable in all the groups, unaffected by the type of medical treatment applied, or by the performance of coronary angioplasty. No further significant change occurred beyond this period. Thus, early thrombolytic therapy does not augment the generally favorable course of recovery of the right ventricle from acute infarction.

Adult↗
PubMed1989

Correlation of baseline plasminogen activator inhibitor activity with patency of the infarct artery after thrombolytic therapy in acute myocardial infarction.

Increased levels of plasminogen activator inhibitor (PAI) have recently been described in patients with acute myocardial infarction (AMI). To correlate PAI levels to patency of infarct arteries after thrombolytic therapy with recombinant tissue-type plasminogen activator (rt-PA), 125 consecutive patients with AMI were examined. Blood levels of fibrinogen, plasminogen, tissue plasminogen activator (t-PA) and PAI were measured before treatment initiation, 10 minutes after completion of rt-PA infusion and 24 and 48 hours after treatment. Coronary angiography, performed in all patients 72 hours after beginning rt-PA infusion, revealed patent infarct arteries in 97 patients and occluded infarct arteries in 28 patients. Pretreatment levels of PAI were significantly higher in patients with occluded infarct arteries (18.0 +/- 11.5 vs 10.5 +/- 9.3 IU/ml, p less than 0.01). Conceivably, higher levels of PAI may interfere with the natural thrombolytic process and make pharmacologic thrombolytic intervention less effective.

Arteries↗
PubMed1989

Abnormal typical pattern of platelet function and thromboxane generation in unstable angina.

Platelet aggregation (PA), platelet thromboxane B2 (TXB2) generation and 14C 5-hydroxytryptamine (5HT) release were studied in 13 patients with unstable angina, and compared to 14 patients with stable angina and 16 healthy controls. A typical pattern, distinct in 4 aspects from stable angina patients or controls, was observed in the unstable angina patients. ADP or collagen induced shape change was 3-4 times greater, the extent of epinephrine induced PA was nil or very low, the extent of collagen induced 14C 5HT release was also reduced while collagen induced platelet TXB2 generation was increased in spite of a reduced extent of PA. The extent of ADP or collagen induced PA was also significantly reduced. These results indicate a platelet membrane abnormality occurring presumably during contact of the circulating platelets with a non-occlusive thrombus observed at sites of ruptured plaques in unstable angina patients. Since also the pattern (20-30% overlap with control values) was distinct from that of stable angina patients, it might indicate an active thrombotic process. Plasma beta-thromboglobulin (beta TG) and TXB2 levels and serum TXB2 generation were also studied in the cardiac patients and controls and in another 10 patients with advanced peripheral occlusive arterial disease (POAD). Plasma beta TG and TXB2 levels were slightly elevated in the unstable angina patients and markedly elevated in the POAD patients. Serum TXB2 generation was, however, elevated in the stable angina patients (p less than 0.002) and more so in the unstable angina patients (p less than 0.001) compared to controls or to POAD patients. This was presumably mediated through enhanced thrombin generation. These results suggest that the measured plasma beta TG variable in the unstable angina patients is not useful in the assessment of in vivo platelet activation. It is presumably reflecting the sum of local enhanced platelet activation (at sites of ruptured plaques) and of reduced function of the "defective" circulating platelets. The ability of the platelets of unstable angina patients to generate large amounts of TXB2 if occurring in vivo might induce an intense coronary vasospasm.

Adult↗
PubMed1989

[Interventional electrophysiology: transcatheter electrical shock ablation for arrhythmias].

Patients with supraventricular or ventricular tachyarrhythmias resistant to antiarrhythmic drugs are candidates for surgical ablation of the bundle of His, and of accessory pathways or ventricular or atrial foci responsible for the arrhythmia. During the past 6 years closed-chest catheter techniques have been devised that allow electrical shock ablation of the atrioventricular junction, accessory pathways, or foci responsible for arrhythmias. The promising results of these ablative procedures (especially of the atrioventricular junction and posteroseptal accessory pathways) justify their trial in suitable patients before cardiac electrosurgery.

Arrhythmias, Cardiac↗
PubMed1989

Dynamics of functional mitral regurgitation during dobutamine therapy in patients with severe congestive heart failure: a Doppler echocardiographic study.

Functional mitral regurgitation plays a major role in determining the therapeutic response to vasodilators in patients with severe congestive heart failure. Its role in the response to inotropic therapy has not been studied in these patients. Ten patients with stage 3 or 4 congestive heart failure (New York Heart Association class) and secondary mitral regurgitation were studied before and during intravenous administration of dobutamine (mean dose, 7.4 microgram/kg/min). Hemodynamic measurements were obtained invasively. Echo and Doppler cardiography were used to determine cardiac volumes. Mitral regurgitation was calculated as the difference between total stroke volume by echo and forward stroke volume by Doppler. Mitral regurgitation area was calculated from a modified hemodynamic formula. Dobutamine caused a marked rise in mean forward stroke volume (43 to 61 ml), with a decrease in mitral regurgitation volume from 20 to 10 ml/beat and a drop in pulmonary capillary wedge pressure from 21 to 13 mm Hg. Since the pressure gradient between the left ventricle and atrium increased significantly during dobutamine therapy, only a marked decrease in the orifice of regurgitation could explain the changes in regurgitant volume. Indeed, the end-diastolic volume decreased from 254 to 234 ml and the orifice of mitral regurgitation was reduced from 0.25 to 0.12 cm2.

Aged↗