Theophylline toxicity after propafenone treatment: evidence for drug interaction.
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Biomedical subjects
Publications and source records attributed to M L Dohrmann.
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The difficulty in interpreting the standard 12-lead electrocardiogram (ECG) due to the interference from muscle potentials produced by arm and leg motion makes it unsuitable during the exercise treadmill test. Likewise, the exercise lead placement ECG cannot substitute for the standard ECG due to significant errors in the former's diagnostic interpretation. This study compares the ECGs recorded via standard and exercise sites regarding frontal and horizontal plane axes, diagnosis and location of myocardial infarction and estimation of infarct size using the complete 54-criteria and 32-point Selvester QRS scoring system. The altered limb lead locations on the exercise ECG caused the QRS vectors to artifactually appear to be directed more inferiorly, posteriorly and rightward, producing a marked rightward mean frontal plane axis shift of +48 degrees (p less than 0.00001). No false positive or false negative anterior infarct was seen on the exercise lead placement ECG, whereas inferior and posterior infarcts were lost in 69% and 31% of patients, respectively. A false lateral infarct was seen in 19% of patients. Estimation of infarct size differed between the 2 ECG sets, with 11 patients increasing their infarct size by 3 to 9% and 14 others decreasing it by 3 to 15% on the exercise lead placement ECG. This study demonstrates that use of body torso positions for limb leads results in substantial QRS waveform variations that disqualify the exercise lead placement ECG as a "standard" recording. Such ECGs should therefore be labeled as "torso positioned" or "nonstandard" to prevent misuse for clinical and investigative purposes.
All patients with chronic stable angina presumed to be due to coronary artery disease should undergo exercise stress testing early in evaluation for evidence of high-risk coronary disease. If the exercise stress test shows early positive findings, patients should undergo cardiac catheterization to exclude left main coronary vessel disease and three-vessel disease with concomitant left ventricular dysfunction. Patients with unstable angina who are subsequently stabilized on medical therapy should undergo a limited exercise stress test before discharge from the hospital to identify those at high risk. An ambulatory ECG is also helpful in evaluating for evidence of silent ischemia in these patients.
To assess the antiarrhythmic efficacy of intravenous propafenone, 20 patients with inducible sustained supraventricular tachycardia received propafenone, 2 mg/kg body weight, or placebo in a double-blind, randomized, crossover study. Three patients had intra-atrial reentrant tachycardia, 3 had atrioventricular nodal reentrant tachycardia, and 14 had atrioventricular reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome. Termination of supraventricular tachycardia occurred in 15 of the 20 patients receiving propafenone but 0 of the 11 patients receiving placebo (p less than 0.01). Propafenone prolonged refractoriness and slowed conduction of the atrium, the atrioventricular node, and accessory atrioventricular bypass tracts, and these effects provided antiarrhythmic action to halt tachycardia. No adverse effects were observed in any patient. We conclude that intravenous propafenone is safe and effective in the acute treatment of various forms of reentrant supraventricular tachycardia.
Our recommendations for the evaluation of the patient with suspected cardiogenic syncope are as follows: An initial thorough history and physical examination of the patient will suggest the diagnosis of cardiogenic syncope in at least 50 per cent of patients. A sudden occurrence of syncope, or "drop attack", is most suggestive of an arrhythmic cause for syncope. If there is no evidence of neurologic, metabolic, or obvious cardiac (for example, aortic stenosis) cause for syncope, a 24-hour ambulatory ECG should be performed. If the patient has had repeated syncopal episodes or if the patient has had seizures that are difficult to control with anticonvulsant therapy, ambulatory ECG monitoring may reveal an arrhythmia in these preselected patients. If the initial 24-hour ambulatory ECG is negative and if the patient has had multiple episodes of syncope, multiple days of recording will be necessary before typical symptoms occur that correlate with arrhythmias. Seventy-two hours of ambulatory ECG monitoring should be sufficient in most instances to establish an arrhythmic cause for syncope. Echocardiography and exercise stress testing are not routinely indicated in the evaluation of syncope unless the clinical history and examination suggest valvular or coronary disease. Rarely, an atrial myxoma will be visualized by echocardiography that is not apparent clinically. Those patients who still have unexplained recurrent syncopal episodes, despite all noninvasive studies, can benefit from invasive electrophysiologic studies, although the expected yield from electrophysiologic testing is low.
Many factors affect the threshold for myocardial stimulation in patients with cardiac pacemakers. The acute local tissue reaction at the electrode-myocardium interface accounts for early threshold rises and may be minimized by choice of specific electrodes (steroid-eluting or carbon-tip). Physiologic variations due to changes in autonomic tone (including eating, sleeping, and exercise) account for day-to-day fluctuations in pacing threshold. Electrolyte and metabolic abnormalities, especially hyperkalemia, alkalosis, acidosis, and hyperglycemia, increase the pacing threshold. Commonly used antiarrhythmic drugs (quinidine and procainamide) also increase pacing threshold. Patients with pacemakers who require antiarrhythmic agents or who have coincident metabolic or electrolyte disturbances should be observed closely for failure to capture. Management of failure to capture is directed at removing the inciting cause and attempting to lower the pacing threshold with isoproterenol, if the situation is urgent. Acute increases in pacing threshold immediately following pacing system implantation can be treated with corticosteroids. Increasing the energy output of programmable pacemakers, in specific circumstances, or insertion of a temporary pacemaker capable of delivering higher energy output than the implanted generator may also be successful.
Eighty men (group A) with clinical coronary artery disease underwent coronary angiography regardless of symptoms and previous therapy because they had a positive treadmill exercise test in stage I or II of the Bruce protocol. Thirty-four other men (group B) who also had an early positive treadmill test underwent coronary angiography because they had disabling angina pectoris despite medical therapy. We found left main coronary artery stenosis of 50% or greater of the vessel diameter in 28% of group A and 35% of group B (p greater than 0.3). In contrast, only 10% of 93 other catheterized patients who had treadmill tests that were not early positive had left main coronary disease (p less than 0.001). Fifty-four patients from group A who did not have left main stenosis of 50% or greater were treated medically. In this subgroup, 85% had 2 or 3 major coronary vessels with 75% or greater stenosis. These patients had a 36 month survival rate of 89.2%. We conclude that an early positive treadmill test identifies patients who have an increased likelihood of having left main coronary stenosis, even if they are minimally symptomatic. To identify left main coronary stenosis, catheterization may be justified in patients whose angina pectoris has been mild or not intensively treated when they have an early positive treadmill response. After left main coronary stenosis has been excluded, these patients may be treated medically with a low mortality.
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We describe a patient with cough syncope who was found to have carotid sinus hypersensitivity with mixed cardioinhibitory and vasodepressor responses. Symptoms were ameliorated by denervation of the more hypersensitive carotid sinus. Spontaneous atypical Wenckebach cycles in this patient were caused by the combined hypersensitive cardioinhibitory and vasodepressor responses. This report stresses the importance of checking blood pressure as well as heart rate in all patients in whom carotid sinus syndrome is suspected.