Showing papers by "Elliott M. Antman published in 1985"

External noninvasive temporary cardiac pacing: clinical trials.

Abstract: An external cardiac pacemaker-monitor has been developed that provides safe, effective noninvasive ventricular stimulation that is well tolerated in conscious patients and allows clear recognition of electrocardiographic response. The noninvasive temporary pacemaker (NTP) has now been applied in 134 patients in five hospitals. Stimulation was tolerated well in 73 of 82 conscious patients, and nine found it intolerable. The NTP was effective in evoking electrocardiographic responses in 105 patients; the 29 failures were in the presence of prolonged hypoxia or severe discomfort. The NTP was clinically useful in 82 patients: 43 of 86 were resuscitated from emergency or expected arrest, 38 of 40 were maintained in standby readiness for up to 1 month but did not require stimulation, and one of eight patients with tachycardia obtained some clinical benefit. The NTP was especially useful in 25 patients with complications or contraindications to endocardial pacing and in 57 patients in whom insertion of an endocardial electrode was avoided.

Use of an ultra short-acting beta-blocker in patients with acute myocardial ischemia.

Abstract: Esmolol is a new ultra short-acting (half-life [t1/2] beta 9 min) beta 1-adrenergic-receptor antagonist reported to have no intrinsic sympathomimetic activity. The safety and efficacy of esmolol in lowering the ventricular rate and rate-pressure product in patients with acute myocardial infarction (n = 5), postmyocardial infarction angina (n = 10), or acute unstable angina (n = 4), and without cardiogenic shock were studied. After a 30 min observation period, esmolol was titrated to a maximum dose of 300 micrograms/kg/min and infused for up to 420 min. The ventricular rate fell from 92 +/- 11 (mean +/- SD) to 77 +/- 13 beats/min (p less than .01) and the systolic arterial pressure decreased from 120 +/- 13 to 97 +/- 11 mm Hg (p less than .01) during the initial 30 min titration period. There was no significant change during the maintenance phase, and both the ventricular rate and arterial pressure returned rapidly toward baseline values within 30 min of termination of the infusion. The cardiac index fell from 2.8 +/- 0.6 to 2.2 +/- 0.6 liters/min/m2 (p less than .01) during the same period, and also returned to the baseline level 30 min after termination of the infusion. There was no significant change in the pulmonary capillary wedge pressure, respiratory rate, or PR interval. Five patients required termination of infusion because of hypotension and all recovered uneventfully within 30 min of stopping the esmolol. One patient required a brief infusion of dopamine to restore hemodynamic stability.(ABSTRACT TRUNCATED AT 250 WORDS)

Experimental and clinical observations on the efficacy of esmolol in myocardial ischemia

Abstract: Beta blockers reduce myocardial oxygen demand and are therefore useful in ischemic states. They reduce angina pectoris and reduce the risk of death when administered long-term after acute myocardial infarction. Some studies suggest that when administered early after coronary occlusion they can reduce myocardial infarct size. Relative contraindications to beta blockers, such as a history of congestive heart failure, chronic obstructive lung disease, atrioventricular conduction defects and low blood pressure, limit their use. Conventional beta blockers have a relatively long duration of action and are either contraindicated or must be used with particular caution in patients with these contraindications. Esmolol is an ultrashort-acting beta blocker with a biologic half-life of 9 minutes. Therefore, such an agent may be useful in patients with ischemic heart disease in whom reducing heart rate would be beneficial but in whom there is concern that beta blockers might not be tolerated. Esmolol reduced myocardial infarct size in 2 experimental studies of coronary occlusion followed by reperfusion, and improved the recovery of the stunned myocardium when administered during experimental myocardial ischemia. Esmolol's brief duration of action may make it safer than conventional beta blockers for the management of patients with unstable angina or myocardial infarction.

Addition of nifedipine to maximal nitrate and beta-adrenoreceptor blocker therapy in coronary artery disease.

Abstract: The effects of oral nifedipine on left ventricular (LV) diastolic function were assessed in 14 patients with coronary artery disease (CAD) who had symptoms despite therapy with beta-adrenoceptor blocking drugs and nitrates. Rest and exercise gated radionuclide ventriculography was performed before and a mean of 13 days after the addition of oral nifedipine (80 to 120 mg/day) to baseline medication. Ejection fraction did not increase in any patient during exercise. The addition of nifedipine slightly improved the LV ejection fraction response to exercise (control, 49 +/- 8% rest vs 44 +/- 9% exercise; nifedipine, 47 +/- 6% vs 48 +/- 8%). With nifedipine treatment, diastolic function improved, with a decrease in the time to peak filling rate (PFR) at rest (from 174 +/- 34 to 152 +/- 31 ms, p less than 0.005) and an increase in PFR with exercise (from 2.5 +/- 0.6 to 3.4 +/- 0.7 end-diastolic volume/s, p less than 0.0005). Using the ratio of PFR/peak ejection rate as a variable, preferential improvement of diastolic over systolic function occurred during exercise (1.03 +/- 0.29 baseline vs 1.4 +/- 0.43 with nifedipine, p less than 0.01). Duration of exercise increased by a mean of 21% with nifedipine (from 454 +/- 150 to 550 +/- 159 seconds, p less than 0.005); all 14 patients were limited by angina pectoris at baseline, whereas only 5 patients were limited by angina pectoris after nifedipine treatment. This study shows that global LV diastolic function is improved by oral nifedipine treatment both at rest and during exercise in patients on maximally tolerated doses of beta-adrenoreceptor blockers and nitrates, and is associated with improvement of symptoms and exercise tolerances.

Pacemaker Malfunction After Nitrous Oxide Anesthesia

Abstract: Entrapment of gas in the pacemaker pocket has been reported. 1,2 Pacemaker malfunction in those studies was a result of loss of anodal contact, and presented with small amplitude, variable amplitude or absent pacing spikes with loss of ventricular capture. We report a patient in whom pacemaker malfunction was caused by the presence of an anesthetic gas within the pacemaker pocket itself.

Pacemaker-Mediated Tachycardia Initiated by Coincident P-Wave Undersensing and Ventricular Blanking Period

Abstract: Pacemaker-mediated tachycardias (PMT) have received much recent attention. We describe the course and treatment of a 60-year-old man with an AV universal (DDD) pacemaker who developed a pacemaker-mediated tachycardia. The tachycardia was initiated by the coincidence of an unsensed P-wave, a QRS that was also not sensed due to the ventricular blanking period, and a short right ventricular myocardial effective refractory period. Treatment consisted of reprogramming the atrial sensitivity of the device. Physicians should be aware of the potential for the ventricular blanking period to participate in the initiation of pacemaker mediated tachycardias.