Shlomo Laniado

Atrial fibrillation and atrial enlargement in patients with mitral stenosis

The present study was designed to assess the relative contribution of atrial fibrillation and left atrial pressure to changes in the size of the left and right atria in patients with mitral stenosis. The study included 155 subjects, 102 of whom underwent prospective echocardiography and Doppler cardiography, and 69 of whom underwent cardiac catheterization. The size of the atria was determined by two-dimensional echocardiography. There were no significant hemodynamic differences between patients with mitral stenosis who were in either sinus rhythm or atrial fibrillation. The left atrium was larger (p less than 0.001) in patients with mitral stenosis and atrial fibrillation (37.6 +/- 10.8 cm2) than in patients in sinus rhythm (27.8 +/- 7.7 cm2) or normal subjects (15 +/- 3.3 cm2). The size of the right atrium was larger (p less than 0.001) in patients with mitral stenosis and atrial fibrillation (21.7 +/- 5.2 cm2) than in patients in sinus rhythm (13.4 +/- 3.9 cm2) or normal subjects (13.8 +/- 3.7 cm2). Multiple regression analysis showed that the severity of mitral stenosis accounted for 38%, age for 7%, and atrial fibrillation for 11% of the change in the size of the left atrium. Atrial fibrillation accounted for 24%, age for 11, and mitral valve area for 3% of the change in the size of the right atrium. The analysis suggests that the onset of left atrial dilatation in mitral stenosis is the result of an early increase in left atrial pressure. Atrial fibrillation, which develops irrespective of the severity of the mitral stenosis, contributes to a further enlargement of the left and right atria.

Randomized controlled trial of late in-hospital angiography and angioplasty versus conservative management after treatment with recombinant tissue-type plasminogen activator in acute myocardial infarction

Although both the European Cooperative Study Group and the Thrombolysis in Myocardial Infarction IIB trial indicated that angiography and angioplasty as routine measures after thrombolytic treatment do not improve clinical outcome in patients with acute myocardial infarction, the potential benefit of angioplasty may have been negated by the fact that the procedure was performed too soon (less than 32 hours) after admission. A similar study was designed in which delayed invasive treatment was compared with conservative treatment in 201 patients with acute myocardial infarction given recombinant tissue-type plasminogen activator. The 97 patients randomized to the invasive group underwent routine coronary angiography and angioplasty 5 +/- 2 days after thrombolytic therapy, whereas the 104 patients randomized to the conservative group underwent angiography only for recurrent postinfarction angina or exercise-induced ischemia. Baseline characteristics of both groups were similar. In the invasive group, 92 patients underwent angiography, 49 angioplasty and 11 coronary artery bypass surgery. In the conservative group, 40 patients experienced early ischemia, 39 underwent angiography, 20 angioplasty and 4 coronary artery bypass surgery. Reinfarction rate and preservation of left ventricular function at discharge or 8 weeks after discharge did not differ in the 2 groups. Total mortality after a mean follow-up of 10 months was 8 of 97 in the invasive and 4 of 104 in the conservative groups (p = 0.15). However, if only patients who died after the timing of the scheduled protocol catheterization in the invasive arm were included, mortality was 5 of 94 and 0 of 100 in the invasive and conservative treatment groups, respectively (p = 0.02). (ABSTRACT TRUNCATED AT 250 WORDS)

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.

Improvement of cardiac performance by intravenous infusion of l-arginine in patients with moderate congestive heart failure

OBJECTIVESnThe aim of this study was to evaluate the hemodynamic effect of L-arginine infusion in patients with congestive heart failure.nnnBACKGROUNDnEndothelium-dependent vasodilation is impaired in patients with congestive heart failure. Nitric oxide, which was identified as endothelium-derived relaxing factor, is generated by nitric oxide synthase from L-arginine. Our hypothesis was that administration of L-arginine in patients with congestive heart failure may increase nitric oxide production and have a beneficial hemodynamic effect.nnnMETHODSnTwelve patients with congestive heart failure (New York Heart Association class II or III) due to coronary artery disease (left ventricular ejection fraction < 35%) were given 20 g of L-arginine by intravenous infusion over 1 h at a constant rate. Stroke volume, cardiac output and left ventricular ejection fraction were determined with Doppler echocardiography at baseline and at 30 and 60 min and 1 h after the end of infusion. Blood and urinary levels of nitrite/nitrate (NO2/NO3), stable metabolites of nitric oxide, were measured and clearance was calculated.nnnRESULTSnOne hour of infusion of L-arginine resulted in a significant increase in stroke volume (from 68 +/- 18 ml to 76 +/- 23 ml [mean +/- SD], p = 0.014) and cardiac output (from 4.07 +/- 1.22 liters/min to 4.7 +/- 1.42 liters/min, p = 0.006) without a change in heart rate. Mean arterial blood pressure decreased (from 102 +/- 11 mm Hg to 89 +/- 9.5 mm Hg, p < 0.002), and systemic vascular resistance decreased significantly. Within 1 h after cessation of L-arginine infusion, blood pressure, stroke volume, cardiac output and systemic vascular resistance were statistically not different from baseline values. Clearance of NO2/NO3 increased significantly during L-arginine administration (from 13.28 +/- 0.42 ml/min to 29.97 +/- 1.09 ml/min, p < 0.001).nnnCONCLUSIONSnInfusion of L-arginine in patients with congestive heart failure results in increased production of nitric oxide, peripheral vasodilation and increased cardiac output, suggesting a beneficial hemodynamic and possibly therapeutic profile.

Improved Survival but not Left Ventricular Function with Early and Prehospital Treatment with Tissue Plasminogen Activator in Acute Myocardial Infarction

One hundred ninety patients with acute myocardial infarction (AMI) were treated with recombinant tissue-type plasminogen activator (rt-PA) 2.0 +/- 0.8 hours after the onset of symptoms. Eighty-seven patients were enrolled via mobile intensive care units and 103 through the emergency ward. Patients who were enrolled via the mobile intensive care units were randomized to immediate, prehospital treatment initiation, or to delayed, in-hospital treatment initiation. All 190 patients except 2 underwent delayed coronary angiography and, when indicated, angioplasty at 72 hours after enrollment. Patients treated within 2 hours and those treated 2 to 4 hours after symptom onset had similar preservation of left ventricular function, and similar prevalence of congestive heart failure at discharge. Patients treated within 2 hours of symptom onset had significantly lower short- (0.0 vs 6.3%, p = 0.01) and long-term (1.0 vs 9.5%, p = 0.03) mortality. Prehospital initiation of rt-PA appeared to be safe and feasible and resulted in a 40-minute decrease in the time from symptom onset to treatment initiation.

Reduction of reinfarction and angina with use of low-molecular-weight heparin therapy after streptokinase (and heparin) in acute myocardial infarction

This study examined whether extending the anticoagulation effect of heparin by low-molecular-weight heparin (clexane) can prevent recurrent myocardial infarction (AMI) treated by streptokinase. On the fifth day after AMI and after heparin therapy cessation, 103 patients were randomly assigned to either treatment with low-molecular-weight heparin (40 mg subcutaneously per day for 25 days, n=43) or control (no treatment, n=60). All patients were followed carefully for 6 months after the infarction date. A total of 32 patients (31%) sustained a cardiac event during the 6-month observation period. There were 12 patients (20%) with reinfarction in the control group versus 2 patients (4.6%) in the low-molecular-weight heparin group during the first 30 days of the study (p=0.02). One additional patient sustained reinfarction at 3 months of followup in the control group, which yielded a total of 13 patients (21.6%) sustaining reinfarction in the control group versus 2 patients (4.6%) in the low-molecular-weight heparin group during 6 months of followup (p=0.01). Angina pectoris after AMI was diagnosed in 13 control patients (21.6%) versus 4 low-molecular-weight heparin-treated patients (9.3%) (p=0.078) during the study period. No major bleeding events were reported in either low-molecular-weight heparin-treated or control patients. Among patients with recently diagnosed AMI treated by streptokinase, extending the anticoagulant effect of heparin for 25 days may prevent recurrent coronary events for at least one month.

Non-invasive recording of late ventricular activity using an advanced method in patients with a damaged mass of ventricular tissue.

Late potentials occurring after the QRS complex were detected on the body surface using an advanced signal averaging technique. ECG waveforms were recorded from patients with and without recurrent ventricular tachycardia who had a damaged mass of ventricular tissue (left ventricular aneurysm or right ventricular dysplasia). The recorded analog data were digitized by a 10 bit A/D converter with a sampling rate of 1280 Hz onto digital magnetic tape. The digitized waveforms were averaged with a CDC-6600 computer using an advanced algorithm which employs a cross correlation function to extract fiducial synchronizing marks for the signal averaging. Waveforms were filtered with a digital bandpass filter with 30 Hz and 250 Hz low and high cut-off frequencies, respectively. Late potentials were detected in seven out of ten patients with left ventricular aneurysm (or right ventricular dysplasia) and recurrent ventricular tachycardia and in four out of five patients with left ventricular aneurysm (or right ventricular dysplasia) but without recurrent ventricular tachycardia. The delayed depolarizations, which were recorded, had an amplitude of 3.0-27.0 microV and extended a mean of 90 msec beyond the termination of the QRS complex. In three patients with left ventricular aneurysm the delayed waveforms were abolished by aneurysmectomy. In nine control subjects no late potentials were detected. We conclude that late potentials which represent late depolarization of a damaged mass of ventricular tissue can be detected in patients with and without recurrent ventricular tachycardia.

Comparative electrophysiologic effects of adenosine triphosphate and adenosine in the canine heart: Influence of atropine, propranolol, vagotomy, dipyridamole and aminophylline

The electrophysiologic effects of adenosine triphosphate (ATP) and adenosine and the modification of these effects by atropine, propranolol, vagotomy, dipyridamole and aminophylline were studied in a canine model. Both ATP and adenosine exerted transient, dose-dependent negative chronotropic and dromotropic effects on the sinoatrial and atrioventricular nodes, respectively. At all doses tested, the effects of ATP were more pronounced. Treatment with either atropine or propranolol plus bilateral cervical vagotomy attenuated the effects of ATP but not of adenosine. In the presence of propranolol plus vagotomy, both the negative chronotropic and dromotropic effects of ATP and adenosine were enhanced and attenuated in a similar manner by dipyridamole and aminophylline. Thus, when ATP and adenosine are injected rapidly into the right atrium of the intact canine heart, vagal involvement in the mechanism of action of ATP but not of adenosine is mainly responsible for the difference in the magnitude of the electrophysiologic effects of these 2 compounds, and only a small part of the electrophysiologic effects of ATP are the result of its degradation to adenosine.

Transcatheter electrical shock ablation of ventricular tachycardia

Transcatheter shock ablation of ventricular tachycardia was attempted in seven patients who had drug-resistant ventricular tachycardia and in one patient in whom ventricular tachycardia was electrophysiologically induced during therapy with multiple antiarrhythmic drugs. Seven patients had previous myocardial infarction and five of them were high risk candidates for surgical therapy. One patient without organic heart disease had repetitive ventricular tachycardia manifesting two different patterns of left bundle branch block. After endocardial mapping, synchronized unipolar 250 to 300 J shocks (one to six) were delivered between the pole recording the earliest endocardial activity during ventricular tachycardia (40 to 200 ms before the onset of the QRS complex) and a body surface electrode. Immediate complications included severe but reversible cardiogenic shock (one patient), nonclinical ventricular tachycardia (two patients, requiring cardioversion in one), transient atrioventricular and intraventricular conduction disturbances (three patients) and permanent left bundle branch block (one patient). A late complication in one patient, left heart failure, occurred 3 days after delivery of five intracardiac shocks. In two patients, left ventricular ejection fraction markedly decreased and in one of them new ventricular contraction abnormalities appeared. Clinical ventricular tachycardia did not recur in five of the seven post-myocardial infarction patients after 7 to 17 months, and it was not inducible in the four patients undergoing late electrophysiologic study. In the patient with idiopathic ventricular tachycardia, one of the configurational types of ventricular tachycardia recurred.(ABSTRACT TRUNCATED AT 250 WORDS)

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)