Premature ventricular complex

One of the more serious complications of magnesium deficiency is cardiac arrhythmias. Premature atrial complexes, atrial tachycardia and fibrillation, ventricular premature complexes, ventricular tachycardia, and ventricular fibrillation may be associated with magnesium deficiency. These effects maybe partly caused by the hypokalemia, renal wasting, and intracellular depletion of potassium caused by hypomagnesemia. 

Primary indications for the use of quinidine include (1) abolition of premature complexes that have an atrial, A-V junctional, or ventricular origin (2) restoration of normal sinus rhythm in atrial flutter and atrial fibrillation after controlling the ventricular rate with digitahs (3) maintenance of normal sinus rhythm after electrical conversion of atrial arrhythmias (4) prophylaxis against arrhythmias associated with electrical countershock (5) termination of ventricular tachycardia and (6) suppression of repetitive tachycardia associated with Wolff-Parkinson-White (WPW) syndrome. 

Moricizine is indicated for the treatment of documented ventricular arrhythmias, particularly sustained ventricular tachycardia. Moricizine was evaluated in the CAST II clinical trial for the prevention of postinfarction ventricular premature complexes. It was ineffective and found to be proarrhythmic. Patients in the moricizine arm of the trial exhibited a greater incidence of sudden cardiac death than did controls. 

Cardiotoxic effects occur most commonly with IV administration and appear as conduction changes (50% widening of QRS complex, frequent ventricular premature contractions, ventricular tachycardia, and complete AV block). 

Kostis JB, Davis D, Kluger J, Aogaichi K, Smith M. Cifenline in the short-term treatment of patients with ventricular premature complexes a double-blind placebo-controlled study. J Cardiovasc Pharmacol 1989 14(l) 88-95. 

Figure 8.25 Exercise test of a patient with doubtful precordial pain and frequent (A) ventricular and (B) supraventricular premature beats. Observe that ST-segment depression was little evident in sinus rhythm complexes, while it was very significant in premature complexes (see V3 and V4 in (B) and V5 and V6 in (A)). (C) The patient presented severe three-vessel disease.

Rasouli ML, Ellestad MH. Usefulness of ST depression in ventricular premature complexes to predict myocardial ischemia. Am J Cardiol 2001 87 891. 

Despite the discouraging results of the CAST, post-MI patients with complex ventricular ectopy remain at risk for death. Other drugs besides type Ic drugs have been studied, including sotalol. Sotalol is marketed as a racemic mixture of a D- and L-isomer both are type in potassium blockers, but the L-isomer has /3-blocking actions. Chronic therapy with D-sotalol was studied in patients with remote MI complicated by complex ectopy in the Survival With Oral D-Sotalol (SWORD) trial. Unlike in the CAST, D-sotalol treatment was not designed to cause PVC suppression, yet (as in the CAST) the trial was halted prematurely because of excessive mortality in the treatment arm. Again, the presumed reason for this observation was D-sotalol-related pro arrhythmia. Currently, only two antiarrhythmic... 

Ruberman W, Weinblatt E, Goldberg JD, Frank CW, Chaudhary BS, Shapiro S. Ventricular premature complexes and sudden death after myocardial infarction. Circulation 1981 64(2) 297-305. 

Salerno DM, Granrud G, Sharicey P, Asii erR, Hodges M A controlled trial of irqxifenone fcr treatment of frequent and repetitive ventricular premature complexes. Am J Cardiol (1984) 53, 77-83. 

Indeca.inide. Indecainide hydrochloride is a po active antiarrhythmic agent that received PDA approval in 1989, but it has not been marketed as of this writing. Chemically, it is 9-[3-(isopropylamino)propyl]fiuorine-9-carboxamide [74517-78-5]. The dmg has potent activity against premature ventricular complexes (PVCs) and ventricular tachycardias. Indecainide has no effect on sinus node function, atrial or ventricular effective refractory periods (32,33). 

Cardiac glycosides have a small ratio of toxic to therapeutic concentration. Possible adverse effects are nausea, vomiting, abdominal pain, diarrhoea, fatigue, headache, drowsiness, colour vision disturbances, sinus bradycardia, premature ventricular complexes, AV-block, bigeminy, atrial tachycardia with AV-Block, ventricular fibrillation. There are several mechanisms relevant for their toxic action (Table 2). 

Ventricular premature depolarizations occur with variable frequency, depending on underlying comorbid conditions. The prevalence of complex or frequent VPDs is approximately 33% and 12% in men with and without CAD, respectively 34 in women, the prevalence of complex or frequent VPDs is 26% and 12% in those with and without CAD, respectively.35 Ventricular premature depolarizations occur more commonly in patients with ischemic heart disease, a history of myocardial infarction, and HF due to LV dysfunction. They may also occur as a result of hypoxia, anemia, and following cardiac surgery. 

Premature ventricular complexes (PVCs) are common ventricular rhythm disturbances that occur in patients with or without heart disease and may be elicited experimentally by abnormal automaticity, triggered activity, or reentrant mechanisms. 

Premature ventricular complexes, 5 88—89 Premature ventricular contractions, 5 108 Premetallized dyes, 9 215-216, 399-401 29 758-759... 

Premature ventricular contractions (PVCs) During conversion or marked reduction in ventricular rate, benign complexes of unusual appearance (sometimes resembling PVCs) may occur after IV verapamil. 

On the basis of two large randomized trials aimed at suppressing premature ventricular complexes after MI, so-called warning arrhythmias, it was discovered that many common antiarrhythmic medications actually increase the risk of mortality [20, 21]. Amiodarone also has been shown to have no definitive effect on mortality in patients after an MI, including in the recent SCD-HeFT trial [22-24]. In fact, of all antiarrhythmic medications, only beta blockers have been clearly shown to prevent SCD after MI [25], particularly among those with depressed LV function [11]. 

Bradycardia, CHF, hypotension, bronchospasm, hypoglycemia, prolonged QT interval, torsades de pointes, ventricular tachycardia, and premature ventricular complexes may occur... 

Electrocardiographic record showing digitalis-induced bigeminy. The complexes marked NSR are normal sinus rhythm beats an inverted T wave and depressed ST segment are present. The complexes marked PVB are premature ventricular beats and are the electrocardiographic manifestations of depolarizations evoked by delayed oscillatory afterpotentials as shown in Figure 13-5. 

Endogenous norepinephrine stimulates cardiac beta receptors. Receptor-linked cAMP-dependent protein kinases phosphorylate calcium channels to increase intracellular calcium. Elevated intracellular calcium increases conduction velocity (phase 0) and decreases the threshold potential in normal SA and AV node cells (see Figure 12.13). Beta blockers slow spontaneous conduction velocity in the SA node by approximately 10-20 percent. In addition, beta blockers can slow conduction velocity while increasing the refractory period of the AV node. These effects control the ventricular rate in atrial fibrillation or flutter and terminate paroxysmal supraventricular tachycardias. They are also safer, although somewhat less effective, than other drugs for suppression of premature ventricular complexes (PVCs). Drugs in this class approved by the FDA for treatment of various arrhythmias include propranolol, acebutolol, and esmolol. Problems with the beta blockers include drowsiness, fatigue, impotence, and depressed ventricular performance. 

The side-effects are associated with vagal effects on the gastrointestinal tract (anorexia, abdominal discomfort/pain, vomiting and diarrhoea), while cardiotoxic effects include premature ventricular depolarizations, nodal rhythms and AV dissociation, Toxicity is enhanced by hypokalaemia, and this may predispose to more complex arrhythmias. 

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