Mr. W, 54, was admitted to the ED with a complaint of "constant chest pressure." He stated that this pressure started approximately 12 hours earlier but it seemed to be getting worse. Mr. W's health history included systemic hypertension and type 2 diabetes. His vital signs on admission were: temporal temperature, 98.6[degrees] F (37[degrees] C); heart rate, 83 beats/minute; respiratory rate, 20 breaths/minute; BP, 181/92; and SpO2, 96% on room air. He was placed on continuous cardiac monitoring, which showed normal sinus rhythm; peripheral venous access was obtained; and specimens for admission lab work, including cardiac biomarkers, were sent to the lab.
Mr. W rated his chest discomfort as an 8/0-10. The pressure was located in the precordial area without radiation; Mr. W was also diaphoretic and nauseated. Evidence-based emergency care for acute coronary syndromes was provided, including aspirin, nitroglycerin, morphine, and a 12-lead ECG.
Mr. W's admission ECG showed an evolving inferior wall myocardial infarction (MI) with pathologic Q waves and ST-segment elevation in leads II, III, and aVF. Because of his worsening chest pressure, self-reported as a "10 out of 10," as well as additional ST-segment elevation in the anterior leads (V3 and V4), the decision was made to take him to the cardiac catheterization lab for reperfusion therapy.
Coronary arteriography demonstrated a 99% stenosis in Mr. W's proximal left anterior descending (LAD) coronary artery, 80% stenosis in the right posterior descending artery, 50% stenosis in the right posterolateral segment, and 60% stenosis in the mid-circumflex artery (See Coronary artery anatomy). Primary percutaneous coronary intervention (PCI) with balloon angioplasty was performed in the LAD artery, with placement of a drug-eluting intracoronary stent. He was admitted to the ICU for monitoring because his left-ventricular ejection fraction (LVEF) was only 35% (normal, 50% to 75%).1 Mr. W had no complaints of discomfort on his first night in the ICU. His post-catheterization ECG showed resolution of the ST-segment elevation.
The next day, Mr. W began to complain of a "slight chest discomfort" that he did not have post-PCI. After notifying the cardiologist, the nurse obtained a stat 12-lead ECG and serum cardiac biomarkers. Mr. W's troponin levels were trending downward, but his ECG (see Mr. W's ECG) concerned his nurse because there was a marked T-wave abnormality seen in the anterior septal (V2-V4) and lateral leads (V5-V6). The T waves "flipped," or inverted, in leads V2, V3, V4, V5, and V6. Based on the new ECG changes and his complaint of new chest discomfort, Mr. W was taken back to the cardiac catheterization lab.
The T wave
The T wave represents ventricular repolarization, and its direction is normally the same as the major deflection of the QRS complex that precedes it.2 T-wave inversion may indicate myocardial ischemia and may also precede the development of ST-segment elevation.2 Based on this information, as well as Mr. W's new complaint of chest discomfort, his healthcare providers were concerned that the newly placed endovascular stent may have occluded.
There are other situations in which deep T-wave inversion may not be indicative of a cardiac ischemic event. T-wave inversion with a prolonged heart-rate corrected QT (QTc) interval can be seen with neurogenic causes such as a subarachnoid hemorrhage.3 Usually, neurogenic T-wave inversion is symmetrical; in review of Mr. W's ECG, he had a prolonged QTc (0.50 second; normal in men, less than 0.43 second), but his T-wave inversion varied in depth and configuration.4 He also did not have any neurologic signs or symptoms. Although Mr. W was not receiving any QT prolonging drugs and did not have any electrolyte abnormalities, QTc prolongation may be caused by underlying heart disease, including heart failure and MI.4
T-wave inversion can also be a sign of myocardial reperfusion, especially if there is a decrease in ST-segment elevation in the early stages of an ST-elevation MI.5 Mr. W was not in the early stages of an MI; his admission ECG showed the presence of pathologic Q waves. Deep, negative T waves with minimal ST-segment elevation in the precordial leads have been reported in patients postreperfusion of a high-grade proximal LAD stenosis.5 This could indicate a high risk for coronary reocclusion, and his healthcare providers were correct to consider urgent coronary arteriography to prevent the progression of myocardial necrosis.
Closing the case
Mr. W's repeat coronary arteriography showed that the newly placed stent was intact and patent. Although Mr. W's original cardiac catheterization demonstrated stenoses in other coronary arteries, he was treated medically. Due to the extent of his disease, he was not considered a candidate for coronary artery bypass graft surgery. Due to his low LVEF and QTc prolongation that was still present at discharge, Mr. W was at increased risk for sudden cardiac death and sent home with a wearable cardioverter-defibrillator and instructions for follow-up care.
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