We describe a patient with ischemically mediated sustained monomorphic ventricular tachycardia occurring at peace and resistant to treatment with intravenously administered procainamide.

We describe a patient with ischemically mediated sustained monomorphic ventricular tachycardia occurring at peace and resistant to treatment with intravenously administered procainamide. Percutaneous transluminal coronary angioplasty was initially prosperous but rest angina and ventricular tachycardia, resistant to procainamide therapy, recurr 2 weeks later and suited to aggressive anti-ischemic medical therapy. We refer to that anti-ischemic medication may be of benefit in patients with malignant ventricular arrhythmias precipitated according to spontaneous myocardial ischemia.

(Chest 1993; 104:1613-14)

Myocardial ischemia is an important trigger factor in the genesis of ventricular arrhythmias and unexpected cardiac death. However, nonfatal ischemically mediated sustained ventricular tachycardia is relatively unusual. Several studies have examined the meanings of myocardial revascularization and anti-ischemic pharmacologic therapy with exercise-induced ventricular arrhythmias.[1-3] Relatively little is known, however, about the validitys of these interventions upon ischemically mediated ventricular arrhythmias unassociated with exercise.

Case Report

A 51-year-old man with atheroselerotic coronary artery disease was hospitalized for crescendo angina. Five month prior to admission, he underwent 2-vessel coronary artery bypass surgery He began receiving metoprolol and isosorbide dinitrate and had done well until 3 weeks prior to admission. After admission to the coronary care unit, he experienced chest discomfort and then exhibited sustained ventricular tachycardia (Fig 1) He re-createed to sinus rhythm when procainamide was administered intravenously. A maintenance infusion was then begun. Coronary arteriography revealed a patent left internal mammary artery graft to the left anterior descending coronary artery, with poor distal runoff. The left circumflex coronary artery was occlud and the obtuse marginal branches were diffusely diseased. The graft to the distal right coronary artery was occlud and there was a filling deficiency presumably thrombus, occluding the origin of the large posterior descending artery Left ventriculography revealed overall normal left ventricular function. Subsequently the patient experienced intermittent chest discomfort followed according to long runs of self-terminating ventricular tachycardia. There was no clear relationship between resting heart rate and the first brunt of the arrhythmia. Percutaneous coronary artery angioplasty at the origin of the posterior descending coronary artery conclusioned in some resolution of run The arrhythmia gradually subsided, and procainamide therapy was discontinued. Electrophysiologic research in the drug-free state, revealed no inducible arrhythmias during programmed stimulation using up to three extrastimuli at pair right ventricular sites and brace paced cycle lengths. Thallium exercise stres experiment showed small fixed defects inferiorly and apically, moreover no reversible defects.

Ten days later, the patient's stay angina recurred, followed by sustained ventricular tachycardia with morphologic findings identical to the original tachycardia. Therapy with intravenously administered procainamide was reinstituted, and because he was a poor interventional candidate, the dosage of metoprolol was increased to 150 mg twice a day and therapy with diltiazem to 360 mg daily, was added. After resolution of the arrhythmia, treatment was switched to the oral form of procainamide, and a repeat electrophysiologic thought again showed no inducible arrhythmias. The exercise stres example was unchanged, and the patient was discharged from the hospital.

The patient was readmitted 6 weeks later because of presum procainamide-induced lupus. Procainamide therapy was discontinued, yet he developed a life-threatening lower gastrointestinal hemorrhage, necessitating crisis transverse colectomy. He experienced no anginal symptoms during this period, and no ventricular arrhythmias were observ After commonplace recovery, he has remained asymptomatic with no further ventricular tachycardia athwart a 9-month period while receiving treatment with metoprolol, diltiazem, and isosorbide dinitrate.

Discussion

There are several factors suggesting that ventricular tachycardia seen in our patient was ischemically mediated. First, it was always preced on typical anginal symptoms. Although ischemic symptoms were not preced at obvious tachycardia, we cannot hinder minor fluctuations in heart rate and family pressure as trigger factors. Alternatively, spontaneous alterations in coronary vasomotor tone may have been responsible. other sustained ventricular tachycardia in patients with ischemic heart disease is inducible with programmed stimulation in greater than 90 percent of cases,[4] while in our patient it was not. Third, the arrhythmia was relatively resistant to anti-arrhythmic medicines but responded dramatically to anti-ischemic therapy, uniform in the setting of life-threatening gastrointestinal hemorrhage. Although ischemically mediated ventricular tachycardia occurring at peacefulness is unusual, ischemic symptoms are belonging to all antecedents to sudden cardiac death, suggesting that this entity many times may be fatal. Perhaps our patient's well-preserved left ventricular function played a part in his favorable outcome. While the experience with antiarrhythmic unsalable articles in the prevention of unusual cardiac death has been disappointing,[5] the beneficial part of beta blockers has been well established.[6] It has become a usual practice to insert automatic implantable cardioverter-defibrillators in patients with sustained ventricular arrhythmias that are not inducible in the electrophysiology laboratory. Our experience refer tos that aggressive anti-ischemic therapy may be of benefit in one of these individuals.

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