Acute ST segment elevation during exercise stress echocardiography due to severe pulmonary hypertension
© Nguyen et al; licensee BioMed Central Ltd. 2011
Received: 21 February 2011
Accepted: 6 June 2011
Published: 6 June 2011
A 51-year-old female undergoing an outpatient stress echocardiogram to evaluate atypical chest pain developed acute ST elevation in the anterior precordial leads on electrocardiogram following exercise. Echocardiography revealed a severe rise in pulmonary artery systolic pressure (PASP) with marked right ventricular (RV) enlargement and interventricular septum flattening. Subsequently, cardiac catherization confirmed an exercise-induced elevation in PASP and diagnosed pulmonary arterial hypertension without evidence of coronary artery disease. This case suggests that an acute elevation in pulmonary artery pressure with RV dilation may be a potential cause of acute ST elevation during stress testing.
Additional file 1: Resting echocardiogram in the parasternal short axis view. Parasternal short axis at rest showing normal LV wall motion and LV systolic function. The RV is mildly to moderately enlarged and hypertrophied. (MPEG 200 KB)
Additional file 2: Resting echocardiogram in the apical 4 chamber view. Apical 4 chamber view at rest showing normal LV wall motion and ejection fraction. The RV is mildly to moderately enlarged and hypertrophied. (MPEG 284 KB)
Acute ST elevation during exercise testing is rare with an incidence of 0.78% in those without prior history of myocardial infarction  and is most commonly secondary to critical proximal LAD obstruction, LV aneurysm, anterior myocardial infarction  and occasionally coronary vasospasm . Our patient demonstrated acute ST segment elevation in the anterior precordial leads with normal coronary arteries on angiography. Mechanism of ST elevation in leads V1-V3 during exercise remains unclear. ST elevation was associated with a marked dilation of RV and development of RV strain pattern on ECG and severe elevation in PASP during exercise. We speculate that sudden pressure load on RV can cause focal or global myocardial ischemia or even injury resulting in ST elevation. Acute RV dilation probably caused RV to displace LV with respect to ECG leads that are fixed on the chest wall. As a result, the anterior precordial leads detected forces that were more prominent from the RV rather than the LV. More prominent right axis deviation as well as increase in P wave height at peak exercise also supports ECG changes secondary to right heart dilation. There was hyperkinetic LV wall motion in all segments which makes vasospasm unlikely and in addition no epicardial artery vasospasm was observed without provocation on coronary angiogram, although we cannot rule out microvascular coronary vasospasm as a cause of ECG changes. Increase in PASP is normally expected during exercise in healthy subjects however peak PASP at exercise does not rise above 43 mm Hg . On RHC, the 10 mmHg decrease in mean PAP following administration of nitric oxide suggests that the pulmonary hypertension was reactive.
ST elevation has been reported in a patient with pulmonary embolism. The mechanism of ST elevation was speculated to be secondary to paradoxical embolization of conus branch of right coronary artery via interatrial shunt in this patient with otherwise normal epicardial coronary arteries . There have been only a few other reported cases of acute RV dilation during exercise stress testing. Acute RV dilation and pulmonary hypertension during exercise was described in a case of pulmonary embolism that was incidentally found on routine stress echocardiogram . Two patients with a history of chronic pulmonary thromboembolism have also been reported to have acute RV dilation following exercise . However, the unique ECG changes associated with RV dilation and an acute severe rise in PAP have not been previously described.
The difference in resting PASP by echo and RHC could be due to underestimation of PASP by resting echo  or an interval progression of pulmonary hypertension during seven weeks between the two procedures as pulmonary hypertension secondary to HIV is more rapidly progressive than idiopathic cases .
Although the most likely etiology of ST elevation in patients undergoing exercise ECG testing is coronary artery disease and rarely coronary vasospasm, our case highlights that an acute severe rise in PAP and associated RV dilation may be another possible cause of ST elevation during stress testing. This awareness will help guide further workup and diagnosis in patients manifesting this phenomenon.
An attempt was made at contacting the patient to obtain consent but the patient could not be reached.
Acknowledgements and Funding
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