Vincenzo Santinelli

Intravenous mexiletine in management of lidocaine-resistant ventricular tachycardia

In coronary care unite, intense activity is directed toward the recognition and suppression of those ventricular arrhythmias which are thought to herald ventricular fibrillation. Ventricular fibrillation is the most common cause of death in the early phase of myocardial infarction, as well as in chronic ischemic heart disease. In some cases it is preceded by ventricular tachycardia, but in others it occurs unexpectedly. Sustained ventricular tachycardia represents a significant problem in the initial care of patients with cardiac disease. Despite comparative safety and effectiveness, lidocaine appears to be less effective during the early phase of acute myocardial infarction.1*2 Although adequate serum levels may often not be achieved with standard doses, in some patients the ventricular arrhythmia appears to be truly “lidocaine resistant.“3*4 Alternative antiarrhythmic drugs, including procainamide, propranolol, and phenytoin, are variably effective. Intravenous disopyramide appears to be an effective antiarrhythmic drug in suppressing serious ventricular arrhythmias, including those not responsive to lidocaine.5 However, the patients with myocardial infarction who have low levels of systemic blood pressure are at increased risk of disopyramide-induced cardiac depression.6*7 Clearly, additional agents are desirable. Mexiletine is a new antiarrhythmic drug, available in oral and intravenous form, that is structurally and electrophysiologically similar to lidocaine. Experimental studies show that it is a quinidine-like drug from group II.8 Clinical studies have shown intravenous mexiletine to be safe and effective in suppressing ventricular arrhythmias that occurred in patients with acute and chronic heart disease as well as in patients with other acute clinical conditions.g-16 This report deals with the clinical evaluation of intravenous mexiletine in a study designed to assess its antiarrhythmic efficacy for emergency treatment of lidoCaine-resistant ventricular tachycardia. A total of 18 patients, 15 men and 3 women, with sustained lidocaine-resistant ventricular tachycardia were entered into the study. Their ages ranged from 40 to 60 years (mean 47 years). Clinical information on these patients is given in Table I. Acute myocardial infarction was present in eight patients; ventricular tachycardia

Ventricular tachyarrhythmias complicating amiodarone therapy in the presence of hypokalemia.

Case I. A 49-year-old woman underwent a mitral commissurotomy in 1977 for mitral stenosis. She was admitted because of syncope. Three months earlier, she began therapy with oral amiodarone (600 mg/day) for control of supraventricular arrhythmia. Two months later, in the absence of hypokalemia, an electrocardiogram (ECG) showed a long QTc interval (600 ms) with a normal QRS duration. Fifteen days before admission, clorthalidone (100 mg every 2 days) was added to amiodarone for mild systemic hypertension. Fifteen days later, syncope due to unusual ventricular tachyarrhythmia occurred (Fig. 1 and 2). At that time the serum potassium level was 3.2 mEq/liter and the tests of thyroid function had normal results. Amiodarone was discontinued. After arrhythmia conversion by intravenous mexiletine, a prolonged QT/U interval (600 ms) was evident.

Paroxysmal Supraventricular Tachycardia: Experience with Propafenone

The authors studied the efficacy of intravenous (IV) (1.5-2 mg/kg) and oral propafenone (450 to 900 mg/day) in 16 patients with paroxysmal, sus tained, recurrent supraventricular tachycardia (SVT). In 5 patients IV propafenone was not given, because of intolerant SVT. Nine patients had Wolff-Parkinson-White syndrome. IV propafenone immediately stopped and prevented reinduction of SVT in 9/11 patients. Oral propa fenone prevented SVT induction in 3 of 5 patients. In the 9 patients re sponsive to IV propafenone, oral pro pafenone was effective: in particular, in 6 patients SVT tachycardia was not induced by serial transesophageal pacings, and in the remaining 3 pa tients the arrhythmia was still in duced but was slower and of brief duration (3-5 seconds). In 11/12 pa tients responsive to oral propafenone the minimum effective dosage in pre venting the induction of the arrhyth mia was 600 mg/day. In only 1 patient was the dose of 450 mg/day equally effective. Propafenone administration was not associated with major side ef fects. In conclusion, propafenone is very effective in the control of parox ysmal supraventricular tachycardia; intravenous propafenone can predict the efficacy of oral therapy.

Sick sinus syndrome: the role of hypervagotonia

A 58-year-old man with persistent symptomatic sinus bradycardia (52 beats/min) showed a markedly prolonged postpacing pause (3240 msec) after atrial pacing at a cycle of 840 msec. In addition, Wenckebach block occurred following atrial pacing at a cycle length of 700 msec. After atropine (2 mg) postpacing pauses returned to normal value and type 1 second-degree AV block completely reversed to 1:1 AV conduction until paced rates greater than 140/min. It may be that in some patients marked and persistent vagal overactivity may predispose to intrinsic sinus node dysfunction; in later stages, sinus node function may paradoxically result unaffected by changes in autonomic tone.

Propafenone in Wolff-Parkinson- White Syndrome at Risk

SummaryWe present our experience on the efficacy of propafenone in ten symptomatic patients with Wolff-Parkinson-White syndrome. The symptoms were dizziness in seven patients and syncope in three patients. While experiencing the symptoms, three of them presented an episode of atrial fibrillation, the shortest preexcited RR intervals being 140, 190, and 200 ms. In the other seven patients, the ECG was not recorded during the symptoms, but an episode of atrial fibrillation was subsequently induced by transesophageal pacing. The shortest preexcited RR intervals during induced atrial fibrillation were 180, 200, 270, 240, 230, 250, and 200 ms. Seven patients had both atrial fibrillation and supraventricular tachycardia. Propafenone (1–2 mg/kg) administered IV in only the patients with sustained atrial fibrillation (spontaneous in two and induced in one patient) prolonged the shortest preexcited RR intervals from 190, 200, and 180 ms to 340, 335, and 340 ms. In the other seven patients, propafenone was not given IV because atrial fibrillation rapidly deteriorated into ventricular fibrillation (one patient) or spontaneously reverted within 1–2 minutes to sinus rhythm (six patients). After oral propafenone, serial trans-esophageal pacing studies reinduced atrial fibrillation in 4 of 6 patients (the shortest preexcited RR intervals increased from 190, 180, 200, and 270 ms to 420, 320, 340, and 380 ms); only in one patient was it possible after propafenone to induce an atrial flutter without preexcitation. After propafenone therapy in 4 of 7 patients, supraventricular tachycardia was not inducible. All patients were asymptomatic during the follow-up period (3–18 months). The minimum therapeutic dosage was 600 mg/day.

Rapid increase of intraventricular conduction delay in the genesis of ventricular fibrillation after atropine

Abstract A 45-year-old man with severe chronic ischemic heart disease, after being given 2 mg total of intravenous atropine for a junctional rhythm of 39–41 beats/min developed heart rate acceleration associated with rapid changes in intraventricular conduction delay to a critical degree so that ventricular fibrillation occurred. This finding supports recent experimental observations that a relationship exists between conduction delay, the rate of change of conduction delay in ischemic myocardium and the initiation of ventricular fibrillation.

Atrial parasystole and amiodarone

On rapporte un cas tres inhabituel de parasystolie auriculaire persistente, etablie par plusieurs enregistrements ambulaires de lECG sur 24 heures, qui a ete traite avec succes par lamiodarone

Are ioxaglate and iopamidol equally safe and well tolerated in cardiac angiography? A randomized, double-blind clinical study.

A randomized, double-blind, parallel-group study was performed in 50 patients undergoing left ventriculography and coronary arteriography to evaluate ECG changes and the effects on left ventricular function of a low-osmolar ionic contrast agent, ioxaglate, as compared with a low-osmolar nonionic contrast medium, iopamidol. Twenty-five patients received ioxaglate (group 1) and 25 patients received iopamidol (group 2). All patients underwent 48 hours of continuous ECG recording beginning 24 hours before the cardiac catheterization. Left ventricular systolic and end-diastolic pressure, peak positive dp/dt, and dp/dt/P ratio were measured immediately before and after left ventriculography and 3 minutes later. Left ventricular systolic pressure did not change after injection of either contrast medium. Left ventricular end-diastolic pressure increased by 30% in group 1 (p less than 0.01) and by 22% in group 2 (p less than 0.01) immediately after left ventriculography. A further increase by 45% in group 1 (p less than 0.01) and by 24% in group 2 (p less than 0.01) was observed 3 minutes later. No differences were observed between values obtained in the two groups. Peak positive dp/dt did not change immediately after injection of either contrast medium but decreased by 5% (not significant) in group 1 and by 7% (p less than 0.02) in group 2 three minutes after left ventriculography. There were no significant differences between the two groups. Analysis of continuous 48-hour ECGs showed that both ioxaglate and iopamidol induced a slight increase (by 8% and 7%, respectively; p less than 0.05) in heart rate during injection with early and complete recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

ST Segment Alternans in Vasospatic Angina

You and your associate^ criticize current pacemaker terminology [particularly in respect of dual demand), and emphasize the importance of clarity in language. It will be difficult to change some terms where usage has become established. It is particularly important therefore that new expressions should be scrutinized with care while there is still time to change any that might be considered confusing. Pacemakers are now coming on the market described as havingdiagnostic functions. Most of these are measurements of pacemaker performance; only a minority give information regarding the function of the patients heart. I would suggest that if a specific term is required to describe the pacemakers ability to measure and report its own function introspective would be a better word than diagnostic. The latter should be reserved for equipment capable of detecting disturbance of the patients cardiac function such as episodes of bradycardia^ and premature beats. Alternatively, thetermdiagnosticmightbe deleted altogether in favor of the general heading Holter functions.

His Purkinje System Conduction and Ventricular Fibrillation in Man

Recently, experimental data from a single canine model in vivo open heart preparation have suggested that fractionation of ventricular activation fronts resulting from the dissociation of the specialized conduction system and the myocardium is one mechanism for the conversion of ventricular tachycardia to ventricular fibrillation. Our recent clinical experience in agreement with these experimental data suggests that the His-Purkinje system may indeed play a role in the genesis of ventricular fibrillation in man. Rapid increase of junctional pacemaker rate following intravenous atropine (2 mg) in a patient with severe ishemic heart disease and junctional rhythm resulted in progressive and marked widening of the QRS complexes (from 0.08 to 0.30 s) so that ventricular fibrillation occurred.^ We suggested that a marked and progressive conduction delay of the His-Purkinje system induced by acute ischemia of the specialized conduction system was probably the cause of both QRS widening and ventricular fibrillation. Indeed, in our case, the heart rate acceleration by itself does not clearly justify the phenomenon; however, a rapid increase in heart rate associated with marked ischemia of the His-Purkinje system may explain both the progressive and marked QRS widening and ventricular fibrillation. Our clinical observation clearly supports the reported experimental data and suggests that the specialized conduction system may indeed play a role in the genesis of ventricular fibrillation in man.