Risk of Stroke After MI
Stroke is an infrequent, early complication of MI, with the reported incidence ranging from 0.7% to 4.7% in the two-week post-MI period. Left ventricular (LV) wall motion aberrations, greater extent of myocardial damage, greater LV dysfunction, and presence of mural thrombi by echocardiography associated with MI have been shown to be associated with an increased short-term risk of stroke. On the other hand, whether MI-induced LV dysfunction is associated with long-term increased risk of stroke has been previously uncertain.
This report examined data from the SAVE trial (Survival and Ventricular Enlargement), in which 2231 patients with MI and LV dysfunction (LV ejection fraction no more than 40%) were followed for an average of 42 months. The estimated overall five-year cumulative stroke rate was 8.1%. In individuals with CT- or MRI-documented stroke, 96% were found to be of ischemic origin.
LV dysfunction was indeed found to be a significant predictive factor for risk of subsequent stroke; there was an 18% increase in risk of stroke for every 5% decrease in LV ejection fraction from that obtained at the time of randomization (i.e., a change from a 35% to a 30% ejection fraction). In particular, individuals with a post-MI ejection fraction of less than 28% has almost twice the risk of subsequent stroke as other patients. Additionally, aspirin was found to reduce the risk of stroke by 56%.
Loh E, et al. N Engl J Med 1997;336: 251-257.
Clinical Scenario: The ECG shown in the figure was obtained from a 30-year-old man with cardiomegaly on chest x-ray and a history of Friedreich’s ataxia. The ECG was obtained because the patient was complaining of palpitations. What is the most likely explanation for the somewhat bizarre findings on this tracing?
Interpretation: The rhythm is sinus at a rate of 90 beats/min. The mean QRS axis is indeterminate since the QRS complex is predominantly negative in both leads I and aVF. There is borderline QRS prolongation (to 0.10 second), with an incomplete right bundle branch block (RBBB) pattern (RsR' in lead V1). In addition, there is biatrial abnormality, persistence of S waves across the precordium, and probable right ventricular hypertrophy (RVH).
Although RAA is usually identified by the presence of tall, peaked P waves in the inferior leads (See Intern Med Alert 1996;18:104), this is one instance when the diagnosis of right atrial abnormality (RAA) is made instead from the finding of a prominent, peaked initial component of the P wave in lead V1. The deep negative component of this P wave suggests concomitant left atrial abnormality (LAA). Putting together the above findings (i.e., RAD, RAA, incomplete RBBB, and persistent S waves), RVH is likely.
Yet even if RVH explains some of the findings on this tracing, one is still left with the QS complex in lead I and the q waves in leads aVL, V5, and V6 that simulate myocardial infarction. This is a bizarre tracing, particularly for an individual who is only 30 years old.
The most reasonable explanation for the presence of cardiomegaly on chest x-ray, a history of cardiac arrhythmias, and an unusual ECG pattern in a young individual is the presence of a cardiomyopathy. In this particular case, the patient had the cardiomyopathy that is associated with Friedreich’s ataxia. This hereditary neurodegenerative disorder commonly involves the heart, producing interstitial fibrosis of the myocardium. Ventricular hypertrophy, congestive heart failure, cor pulmonale, and/or cardiac arrhythmias result. The cardiomyopathy is progressive and is often the cause of death. Other heredofamilial neuromyopathic disorders that may involve the heart include the progressive muscular dystrophies (Duchenne’s dystrophy) and myotonic muscular dystrophy.
Cardiomyopaathies may produce any of a diverse group of ECG abnormalities including left or right ventricular hypertrophy, LAA or RAA, interventricular conduction blocks (including LAHB, LBBB, RBBB, and nonspecific intraventricular conduction defect)and/or any of the above in combination.