Original Article
Life-Threatening Ventricular Arrhythmias in Patients with Silent Myocardial Ischemia Due to Coronary Artery Spasm
N Engl J Med 1992; 326:1451-1455May 28, 1992
- Abstract
- Abstract
Background
Silent myocardial ischemia in patients with coronary atherosclerosis is associated with an increased risk of adverse cardiac events, including sudden death. The relation between silent ischemia and the initiation of potentially fatal ventricular arrhythmias has not been defined, however.
Methods
As part of a long-term study of sudden cardiac death, data on arrhythmias, coronary anatomy, and responses to ergonovine testing to provoke coronary artery spasm were collected prospectively among survivors of out-of-hospital cardiac arrest who had no flow-limiting coronary artery lesions, prior myocardial infarctions, or other structural causes of cardiac arrest and no angina pectoris. Associations between silent myocardial ischemia due to coronary artery spasm and the occurrence and characteristics of life-threatening ventricular arrhythmias were studied by both invasive and noninvasive techniques.
Results
Silent ischemic events were associated with the initiation of life-threatening ventricular arrhythmias in five patients with induced or spontaneous focal coronary artery spasm (or both). These patients were identified among a group of 356 survivors of out-of-hospital cardiac arrest who were evaluated between 1980 and 1991. In two of the five patients reperfusion, rather than ischemia itself, correlated with the onset of the ventricular arrhythmia. Only one of the five had an inducible arrhythmia during electrophysiologic testing. Titration of the dose of a calcium-entry—blocking agent (verapamil, diltiazem, or nifedipine) against the ability of ergonovine to provoke spasm was successful in preventing both the provocation of spasm and arrhythmias in all four patients who were tested.
Conclusions
Silent myocardial ischemia due to coronary artery spasm can initiate potentially fatal arrhythmias in patients without flow-limiting structural coronary artery lesions. The role of silent ischemia, reperfusion, or both in the initiation of fatal arrhythmias in larger groups of patients with advanced coronary artery lesions remains to be defined. (N Engl J Med 1992;326:1451–5.)
Media in This Article
Figure 1
Arrhythmia during Silent Ischemia and Reperfusion.Figure 2
Coronary Angiogram Obtained during Ergonovine-Induced Spasm.Article Activity
- Article
The clinical importance of shifts in ST segments of the electrocardiogram that are unaccompanied by angina pectoris or anginal equivalents (silent myocardial ischemia) is a topic of considerable interest and debate.1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Patients who have silent (asymptomatic) ST-segment shifts and coexisting coronary disease are at increased risk for adverse cardiac events,8 , 9 , 11 12 13 14 , 16 including sudden death.11 12 13 14 , 16 In addition, sudden death may result from coronary artery spasm, with or without pain.17 18 19 20 21 22 The relation between silent myocardial ischemia and potentially fatal arrhythmias has not been well defined, however.13 , 14 , 16 Since both are transient pathophysiologic events, correlative data have been accumulated only from incidental ambulatory-monitor recordings23 24 25 or by the demonstration of exercise-induced silent ischemia in survivors of cardiac arrest.26 27 28 29 In this report, we describe a direct association among coronary artery spasm, marked degrees of silent myocardial ischemia, and the onset and mechanisms of potentially fatal ventricular arrhythmias in five survivors of cardiac arrest.
Methods
The five patients were evaluated at the University of Miami Medical Center between 1980 and 1991 after surviving out-of-hospital cardiac arrests. The observations in the first patient, published in part elsewhere,30 led to the establishment of criteria for subsequent patients to be evaluated. The criteria included: (1) cardiac arrest with documented ventricular fibrillation or sustained ventricular tachycardia; (2) the absence of angina pectoris or acute myocardial infarction at the time of the index event, and of prior myocardial infarction or angina pectoris; (3) normal left ventricular ejection fraction and wall motion; (4) the absence of coronary artery lesions causing stenosis of ≥50 percent; and (5) no other (noncoronary) cardiac abnormalities. The patients who met these criteria for the absence of structural heart disease as a basis for cardiac arrest during complete clinical, hemodynamic, angiographic, and electrophysiologic studies were also evaluated by continuous electrocardiographic monitoring for spontaneous shifts in the ST segment and associated arrhythmias, and by ergonovine provocation unless contraindicated. In 5 of the 13 patients who met the criteria, we documented silent ischemia associated with potentially fatal arrhythmias.
All the patients were continuously monitored with leads II and MCL-1, and the documentation of spontaneous arrhythmias was retrieved from a computerized storage system. Ischemia during bedside monitoring was defined as either an ST-segment elevation or a horizontal or downsloping ST-segment depression of ≥1 mm, measured 80 msec after the J-point and lasting for 1 minute or more. Among the four patients who had positive results on ergonovine testing, repeated provocation studies were performed against titrated doses of a calcium-entry blocker or blockers (verapamil, diltiazem, or nifedipine) in an attempt to prevent the reinduction of spasm. The ergonovine studies, during which the patients were continuously monitored for ST shifts and arrhythmias, began with an initial dose of 0.025 or 0.05 mg, with incremental increases until focal spasm occurred or a maximal dose of 0.40 mg was reached. No calcium blocker, beta-adrenoceptor blocker, or membrane-active antiarrhythmic drugs were given at the time of the initial ergonovine provocation. After the dose of ergonovine required to induce spasm had been established in the initial angiographic study, the patients received a calcium-entry blocker and were studied again after five or more doses. If spasm was still inducible at the same dose of ergonovine, the dose of the calcium blocker was increased and the patient was studied again. This procedure continued until spasm could not be induced by a dose of ergonovine higher than that responsible for the initial spasm.
Case Reports
Patient 1
Patient 1 was a 56-year-old man who had recurrent ventricular tachycardia and ventricular fibrillation accompanied by asymptomatic anterior ST-segment elevations. Angiographically, he had a lesion causing 30 percent stenosis in the left anterior descending coronary artery. Ergonovine provoked critical narrowing, and nitroglycerin reversed the spasm. Verapamil, titrated to a dosage of 160 mg every six hours, prevented its reinduction. There were no further arrhythmic events during 32 months of follow-up.
Patient 2
Patient 2 was a 49-year-old man who collapsed while jogging. Ventricular fibrillation, which spontaneously reverted to atrial fibrillation, was recorded by rescue personnel. In the hospital, spontaneous shifts in the ST segment were accompanied by runs of nonsustained ventricular tachycardia; some were followed by rapid polymorphic ventricular tachycardia with loss of consciousness. Reversible, nearly total obstruction of the proximal right coronary artery occurred, both spontaneously and in response to ergonovine provocation. During nitroglycerin-induced reperfusion there were two episodes of rapid polymorphic ventricular tachycardia. Both converted spontaneously, revealing underlying atrial fibrillation (Fig. 1Figure 1
Arrhythmia during Silent Ischemia and Reperfusion.). Nifedipine and diltiazem in combination prevented the reinduction of spasm by ergonovine, and the patient remained event-free during 64 months of follow-up.Patient 3
Patient 3 was a 47-year-old man who collapsed while jogging and was found to be in ventricular fibrillation. His cardiac rhythm was atrial fibrillation after defibrillation was performed, and it had reverted to sinus rhythm on his arrival at the hospital. Coronary angiography revealed a lesion causing 25 percent stenosis in the left anterior descending coronary artery distal to several septal perforator branches. Ergonovine provocation induced critical focal constriction of the left anterior descending coronary artery and mild diffuse narrowing (Fig. 2Figure 2
Coronary Angiogram Obtained during Ergonovine-Induced Spasm.A) accompanied by nonsustained ventricular tachycardia at a cycle length of 220 msec. Diltiazem in a dose of 60 mg every six hours prevented the reinduction of critical spasm (Fig. 2B). There were no further events during 36 months of follow-up.Patient 4
Patient 4 was a 43-year-old man who collapsed while engaged in nonstressful activities. Defibrillation successfully converted his cardiac rhythm from ventricular fibrillation. In the hospital, an episode of silent ischemia was accompanied by irregular, nonsustained polymorphic ventricular tachycardia (cycle length, 190 to 230 msec). Ergonovine induced reversible, nearly total obliteration of the circumflex artery and an intermediate ramus branch, with additional diffuse narrowing of the left anterior descending arterial system. Spasm could not be reinduced with a regimen of 60 mg of diltiazem every six hours. The patient remained event-free during 12 months of follow-up.
Patient 5
Patient 5 was a 68-year-old woman who had a cardiac arrest caused by ventricular fibrillation while speaking on the telephone. After she was resuscitated, coronary angiography revealed a lesion causing 25 percent stenosis in the left main coronary artery, with evidence of spontaneous spasm. Ergonovine provocation was not performed. During monitoring, a painless shift in the ST segment was followed by spontaneous rapid polymorphic ventricular tachycardia that further degenerated to ventricular fibrillation. During electrophysiologic testing, ventricular flutter was induced and terminated spontaneously. Oral propranolol failed to prevent inducibility of the ventricular arrhythmias, and the patient received an implantable defibrillator.
Results
Clinical Data
Between 1980 and 1991, 356 survivors of out-of-hospital cardiac arrest were evaluated. Among the 13 patients without an identifiable explanation for cardiac arrest during the initial workup, 5 were found to have the combination of coronary artery spasm, silent myocardial ischemia, and documented ventricular arrhythmias related to ischemia or reperfusion (Table 1Table 1
Demographic and Clinical Characteristics of Five Patients with Silent Myocardial Ischemia.*). The mean (±SD) age of the 5 patients was younger than that of the overall group of 356 (53±9 vs. 62±10 years), but did not differ markedly from the other 8 without either structural heart disease or silent ischemia (mean age, 51 ±12 years). Patient 4 had a history of atypical chest pain, but none of the patients had pain at the time of the cardiac arrest or during subsequent spontaneous or induced ischemia. One (Patient 3) was a cigarette smoker. Patients 3 and 5 were receiving a beta-blocker, and none were taking vasoactive, calcium-blocking, or antiarrhythmic drugs.All the patients had silent ischemia documented in the hospital. Three had both spontaneous and ergonovine-provoked silent ischemia, one had only spontaneous ischemia (no provocation study was performed), and one had only ergonovine-induced silent ischemia. Patients 1, 2, and 5 had sustained ventricular tachycardia or ventricular fibrillation associated with spontaneous silent ischemia, and Patient 4 had nonsustained rapid polymorphic ventricular tachycardia. Ventricular arrhythmias accompanied ergonovine-induced silent ischemia in Patients 1, 2, 3, and 4. All the tachyarrhythmias were at rapid rates, with cycle lengths ≤240 msec. Polymorphic ventricular tachycardia, ventricular flutter, and degeneration to ventricular fibrillation were all recorded. No patient had slower, hemodynamically stable monomorphic ventricular tachycardia. All the patients had normal left ventricular ejection fractions, left ventricular filling pressures, and cardiac indexes. None had flow-limiting coronary lesions or electrocardiographic or angiographic evidence of a prior myocardial infarction. Patients 2, 3, and 4 had treadmill stress tests with thallium imaging; each was negative. No patient had other diseases, although Patient 5 had been treated for Hodgkin's disease more than 20 years earlier.
Electrophysiologic Testing
Only Patient 5 had an inducible ventricular arrhythmia during electrophysiologic testing. Self-terminating ventricular flutter that resulted in a fall in blood pressure was induced by three extrastimuli; the cycle length was <200 msec.
Induced Spasm and Arrhythmias during Ergonovine Provocation
Among the four patients who received ergonovine for provocation studies, two had sustained ventricular tachycardia or ventricular fibrillation after provoked silent ischemia (Patient 1 during ischemia and Patient 2 during reperfusion), and two had runs of rapid polymorphic nonsustained ventricular tachycardia (Patient 4 during ischemia and Patient 3 during reperfusion). Figure 2 shows angiographic frames recorded in Patient 3 during ergonovine-induced spasm (Panel A) and during the prevention of induced spasm by diltiazem (Panel B). The patient had runs of nonsustained polymorphic ventricular tachycardia during reperfusion after he received nitroglycerin following induced spasm. The titration protocol for the calcium blocker prevented the reinduction of critical spasm in all four patients in whom it was attempted, and no further silent ischemia or arrhythmias were observed.
Atrial Fibrillation after Ventricular Fibrillation
The termination of one or more episodes of ventricular arrhythmia revealed the presence of atrial fibrillation in four patients, two of whom had a documented absence of atrial fibrillation on monitor data immediately beforehand (Fig. 1). In the other two patients, there was no history of atrial fibrillation, but it was present after defibrillation. The mechanism for an association between ischemic ventricular tachycardia or ventricular fibrillation and atrial fibrillation is unknown.
Discussion
Transient myocardial ischemia may be the triggering mechanism for fatal ventricular arrhythmias in some victims of cardiac arrest.31 32 33 Although anti-ischemic therapies appear to protect against recurrences in patients with identified ischemic mechanisms,32 , 34 the relative importance of ischemia and structural abnormalities (e.g., ventricular aneurysms, prior infarctions, or left ventricular hypertrophy) may be difficult to distinguish, especially in the absence of symptomatic ischemia.32 , 33 , 35 , 36 In this report, we establish a relation between silent ischemia due to coronary artery spasm and potentially fatal ventricular arrhythmias in patients without confounding structural heart disease. These observations demonstrate that when it is severe, silent transient ischemia may initiate fatal arrhythmias in the absence of high-grade coronary lesions or old or recent infarctions. The patients described here constitute a small and select subgroup of a large number of survivors of cardiac arrest, but the same mechanism could operate in larger groups with more complex pathophysiologic features. The risk associated with the severity of ischemia reported here must be distinguished from that associated with the mild subendocardial silent ischemia that may occur in patients with chronic stable angina; the various types of painless ischemia are probably not equally dangerous.
Among patients who have a primary ischemic mechanism for cardiac arrest, with or without concomitant structural heart disease, ventricular tachycardias tend to be rapid (cycle length, ≤240 msec) and may have polymorphic or ventricular-flutter patterns. Rapid degeneration of the rhythm to ventricular fibrillation is common. However, sustained ventricular tachycardia is often not inducible during electrophysiologic studies. In contrast, when underlying heart disease creates the structural environment for a reentrant mechanism for the arrhythmia, sustained ventricular tachycardia is usually slower, monomorphic, and more stable, and it is usually inducible during electrophysiologic testing. Nonetheless, coronary angiography may also reveal the presence of lesions that could be expected to produce sufficient ischemia to alter the chronically abnormal arrhythmogenic substrate. Metabolic studies of lactate production during programmed-stimulation studies have supported a role of ischemia.33 When ischemia is clinically silent, however, its role may be underestimated.
Both silent ischemia37 and coronary spasm38 , 39 may be induced during exercise, and it is noteworthy that two of the patients in this report had cardiac arrest while jogging. Two reports cite associations between prior ventricular fibrillation and silent ischemia during exercise testing.26 , 29
Although ischemia generates electrophysiologic changes that can initiate fatal arrhythmias,35 at least two patients in this report (Patients 2 and 3) had potentially fatal arrhythmias during myocardial reperfusion after a period of ischemia. In experimental studies,40 , 41 reperfusion arrhythmias after 10 or more minutes of ischemia tend to be rapid, polymorphic, and self-terminating, similar to those observed in three of the patients in this report. They may be related to calcium overload due to ischemic injury,42 with triggered activity as a possible mechanism. Triggered activity refers to a cardiac arrhythmia evoked by electrical oscillations of cell membranes ("afterdepolarizations"), during or after repolarization. Calcium currents appear to be involved.
Since three of the four patients who underwent ergonovine testing with calcium-blocker titration required more than one dose level of calcium blocker to prevent the reinduction of spasm, we were able to document that the induction of spasm was reproducible at similar doses of ergonovine. Nonetheless, to determine the final doses of calcium blockers, we required the prevention of flow-limiting spasm at a dose of ergonovine higher than that required to induce spasm initially. Although this strategy was successful in all four patients in whom it was tried, with all remaining event-free during follow-up, it is important to emphasize that this outcome does not necessarily have a bearing on long-term survival. Without randomized control data, the only firm conclusion is that treatment was effective over the short term in preventing ergonovine-inducible spasm and related arrhythmias.
If these data are supported in larger and more general populations, the principle that silent ischemia may be arrhythmogenic provides a previously unrecognized additional justification for intensive anti-ischemic therapy in patients with silent ischemia who are at risk for potentially fatal ventricular arrhythmias. It also suggests that ergonovine testing may be useful in survivors of cardiac arrest who have no flow-limiting coronary artery stenoses.
Supported in part by a grant (HL-28130) from the National Heart, Lung, and Blood Institute.
We are indebted to Ms. Thelma L. Gottlieb for assistance in the preparation of the manuscript and to Lynne Pringle, R.N., for assistance in data retrieval and collation.
Source Information
From the Division of Cardiology, Department of Medicine, University of Miami School of Medicine (R.J.M., K.M.K., S.M.M., M.M.C., E.D., A.I., A.C.), and the Miami Veterans Affairs Medical Center (K.M.K.), both in Miami. Address reprint requests to Dr. Myerburg at the Division of Cardiology (D-39), University of Miami School of Medicine, P.O. Box 016960, Miami, FL 33101.
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