Alternans of the ST Segment and T Wave. A Sign of Electrical Instability in Prinzmetal's Angina

Rozanski, John J.; Kleinfeld, Morris

doi:10.1111/j.1540-8159.1982.tb02243.x

Cited by 55 publications

(22 citation statements)

References 14 publications

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“…4,5 STEA is a rare entity, occurring in up to one third of patients with Prinzmetal angina. 2 STEA has been shown to be a harbinger of ventricular tachycardia or fibrillation, occurring with severe myocardial ischemia at the moment of maximal ST-segment elevation, specifically involving the left anterior descending artery territory. 2,3,5 STEA is associated with a longer duration of ischemia, and in some reports, it has always preceded ventricular arrhythmia.…”

mentioning

confidence: 99%

ST-Elevation Alternans and Nonsustained Polymorphic Ventricular Tachycardia in a Patient With Prinzmetal (Variant) Angina

Shah

Januzzi

2010

Circulation

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A 62-year-old man with a prior history of smoking, lung cancer (treated with chest radiation and lobectomy 4 years before admission), and hyperlipidemia presented to our hospital with 4 episodes of substernal chest pressure radiating to his left upper arm. The pain was associated with dyspnea and lightheadedness and resolved after a characteristic period of 10 minutes. The pain was not related to time of day or stress. He performed aerobic exercise regularly without clear precipitation of chest discomfort. His family and social history were unremarkable. His baseline ECG is shown in Figure 1.After serial testing for cardiac troponin was negative, the patient underwent a routine exercise treadmill test with a standard Bruce protocol. At 2 minutes 50 seconds into the treadmill test, he experienced crushing substernal chest pressure, typical of his prior episodes, in association with significant ST-segment elevation throughout his anterior precordium (Figure 2). He experienced dyspnea, diaphoresis, and lightheadedness, and sublingual and intravenous nitroglycerin were administered immediately. At 1 minute into his recovery period, he had nonsustained polymorphic ventricular tachycardia (Figure 3). The ST-segment elevations persisted to 7 minutes into recovery before full resolution.He was taken urgently to our cardiac catheterization laboratory, where a minimal plaque in his proximal left anterior descending artery was demonstrated (Figure 4), with minimal other disease, which supports a diagnosis of Prinzmetal (variant) angina as the cause of his profound ST-segment deviation during exercise. A closer inspection of his stress ECG (Figures 2 and 3) revealed ST-elevation alternans (STEA), a very rare phenomenon previously

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confidence: 99%

ST-Elevation Alternans and Nonsustained Polymorphic Ventricular Tachycardia in a Patient With Prinzmetal (Variant) Angina

Shah

Januzzi

2010

Circulation

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“…Visible alternation in the amplitude of the T wave (T-wave alternans, TWA) is a rare but significant finding that has been associated with malignant ventricular arrhythmias. 2,3 Recently, a method was developed to detect more subtle microvolt levels of TWA. 4 -6 Microvolt TWA was subsequently shown to be associated with inducible ventricular arrhythmias during electrophysiological studies as well as spontaneous arrhythmic events.…”

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confidence: 99%

Effects of Selective Autonomic Blockade on T-Wave Alternans in Humans

et al. 2002

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Background-T-wave alternans (TWA) is an important noninvasive measure of ventricular arrhythmia vulnerability. This study tested the hypothesis that the autonomic nervous system influences TWA measurement in high-risk subjects with coronary artery disease. Methods and Results-T-wave alternans was measured in 60 patients with coronary artery disease, left ventricular dysfunction, and inducible sustained ventricular tachycardia during electrophysiological studies. All patients had TWA measured at baseline with atrial pacing at 100 bpm (600 ms), 109 bpm (550 ms), and 120 bpm (500 ms). After a 10-minute recovery period, TWA was measured again after sympathetic blockade (esmolol, nϭ20), parasympathetic blockade (atropine, nϭ20), or no intervention (control subjects, nϭ20). The prevalence of significant TWA was unchanged compared with baseline after atropine infusion and in the control group. In contrast, the amplitude of TWA in the vector magnitude lead was significantly reduced after esmolol infusion (PϽ0.001), and the number of positive TWA tests was reduced by 50% (70% versus 35%, PϽ0.05). Conclusions-Our findings have important implications for the use of TWA to risk-stratify patients for life-threatening ventricular arrhythmias and provide a new potential mechanism for the reduction in sudden cardiac death conferred by ␤-blockers among patients with coronary artery disease and congestive heart failure.

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“…This same process leads to wave-front fractionation and thus predisposes to reentrant ventricular dysrhythmias. Electrical alternans has been reported to precede ventricular dysrhythmias (12). It has also been reported to precede ventricular fibrillation in dogs undergoing coro- nary artery ligation (13).…”

Section: Resultsmentioning

confidence: 99%

Simple finite-element model accounts for wide range of cardiac dysrhythmias.

Smith¹,

Cohen²

1984

Proc. Natl. Acad. Sci. U.S.A.

140

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A simple finite-element model of ventricular conduction processes that explicitly incorporates spatial dispersion of refractoriness was developed. This model revealed that spatial dispersion of refractoriness is a sufficient condition to produce self-sustained reentry even in the absence of unidirectional block, inhomogeneity in local conduction velocities, or the presence of ectopic pacemakers. The model displayed a wide variety of rhythm disturbances qualitatively similar to clinically familiar cardiac dysrhythmias. Electrical stability of the model was determined as a function of the model parameters including ventricular stimulation rate, conduction velocity, and mean refractory period as well as standard deviation of refractory periods. We conclude that spatial dispersion of refractoriness is a sufficient condition to initiate reentrant dysrhythmias but that other physiologic variables such as ventricular rate and conduction velocity strongly influence the dysrhythmogenic effect of spatial dispersion of refractoriness.Over the past 20 years, a unified hypothesis concerning the mechanism of reentrant cardiac rhythm disturbances has been developed (1-4). The "dispersion of refractoriness" hypothesis is rooted in the concept that the spread of depolarization over myocardial tissue is fundamentally a synchronous process in which activation of one region of tissue spreads to activate neighboring regions. The process of repolarization, on the other hand, is fundamentally an asynchronous process in which local clocks determine the length of time during which a region of tissue remains depolarized and thus refractory to further stimulation. Spatial variation in refractory times leads to the appearance of islands of refractory tissue during the repolarization process ( Fig. 1). A new wave of depolarization impinging on these islands of refractory tissue will fractionate. Such fractionation of the depolarization wave front can lead to eddies and reentry. These processes can lead to a variety of disturbances of heart rhythm, including single or multiple premature depolarizations, sustained tachydysrhythmias, and, ultimately, fibrillation. Fibrillation represents a completely chaotic turbulent pattern of local reentrant activity.One may generalize the dispersion of refractoriness hypothesis to include not only spatial dispersion of refractory times but all factors that predispose to variability in the spatial coherence and temporal synchronization of the repolarization process. Variations in the local electrical properties of the myocardium (e.g., refractory period, conduction velocity) will predispose to "spatiotemporal dispersion of refractoriness" and, thus, to reentry.This hypothesis is attractive in that it provides a simple conceptual basis for understanding a wide range of observations regarding factors that predispose or provoke reentrant cardiac dysrhythmias including fibrillation. For example, electrical stimulation of the ventricular myocardium during the "vulnerable period," which roughly correspond...

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Alternans of the ST Segment and T Wave. A Sign of Electrical Instability in Prinzmetal's Angina

Cited by 55 publications

References 14 publications

ST-Elevation Alternans and Nonsustained Polymorphic Ventricular Tachycardia in a Patient With Prinzmetal (Variant) Angina

ST-Elevation Alternans and Nonsustained Polymorphic Ventricular Tachycardia in a Patient With Prinzmetal (Variant) Angina

Effects of Selective Autonomic Blockade on T-Wave Alternans in Humans

Simple finite-element model accounts for wide range of cardiac dysrhythmias.

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