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Transient ST-Segment Elevation Following Coronary Artery Bypass Grafting in a Patient With Immune Thrombocytopenia Treated With Romiplostim: A Case Report

This case report describes a clinically stable patient with immune thrombocytopenia treated with romiplostim who developed transient postoperative ST-segment elevation following CABG that was ultimately attributed to post-pericardiotomy pericarditis rather than myocardial infarction, highlighting the importance of individualized evaluation to avoid unnecessary invasive procedures in such complex cases.

Original authors: Zakiur Rehman Ansari, Zainul Abedein Hamdulay, Azizullah Khan, Sanjesh Jain, Meher Hamdulay, Aziz Kothawala

Published 2026-08-21
📖 7 min read🧠 Deep dive

Original authors: Zakiur Rehman Ansari, Zainul Abedein Hamdulay, Azizullah Khan, Sanjesh Jain, Meher Hamdulay, Aziz Kothawala

Original paper licensed under CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). This is an AI-generated explanation of the paper below. It is not written or endorsed by the authors. For technical accuracy, refer to the original paper. Read full disclaimer

When the heart is opened for surgery, the body reacts with a complex mix of healing and inflammation. One of the most critical tools doctors use to monitor a patient after heart surgery is an electrocardiogram, a test that records the heart's electrical rhythm. On this recording, a specific pattern called ST-segment elevation often appears. In the days following a major operation like a coronary artery bypass, where surgeons reroute blood flow around blocked arteries, this pattern usually raises an alarm. It frequently signals that a new graft has failed or that the heart muscle is suffering from a lack of oxygen, a condition known as a heart attack. Because these situations are life-threatening, the standard response is often to rush the patient back for an invasive procedure to look inside the arteries. However, the heart does not always behave the same way after surgery. Sometimes, the body's natural response to the trauma of cutting into the chest wall and the heart itself creates inflammation that mimics a heart attack on the monitor, even when the blood vessels are open and working perfectly. Distinguishing between a true emergency and a temporary inflammatory reaction is difficult, but getting it wrong can lead to unnecessary risks, especially for patients who already have fragile blood clotting systems.

This challenge becomes even more intricate when a patient has a condition called immune thrombocytopenia. This is a disorder where the body's immune system mistakenly destroys its own platelets, the tiny cells responsible for forming clots to stop bleeding. Patients with this condition have low platelet counts, which makes any surgery dangerous because of the high risk of uncontrolled bleeding. To prepare such a patient for heart surgery, doctors often use a medication called romiplostim. This drug acts like a signal to the bone marrow, telling it to produce more platelets quickly so the patient can survive the operation safely. While this treatment is effective at raising platelet numbers, it introduces a new layer of complexity. Because the drug forces the body to make more clotting cells, there is a theoretical concern that it might also increase the risk of dangerous clots forming in the heart or blood vessels. When a patient with this specific background undergoes heart surgery and then shows signs of distress on an electrocardiogram, doctors face a difficult puzzle. They must decide whether the heart is in immediate danger from a blocked vessel or if the signal is a false alarm caused by inflammation, all while balancing the risks of bleeding from too few platelets and clotting from too many.

A team of surgeons and cardiologists at Masina Heart Institute in Mumbai recently documented a case that illustrates this delicate balancing act. The patient was a 47-year-old man who had suffered from chronic immune thrombocytopenia for five years and also had severe blockages in three major arteries of his heart. Before his scheduled surgery to bypass these blockages, his medical team administered a dose of romiplostim to boost his platelet count. The treatment worked, raising his platelet levels enough to allow the surgery to proceed safely. The operation itself went smoothly, and the patient recovered well in the immediate hours afterward. However, on the first day following the surgery, a routine check of his heart rhythm revealed a new and worrying pattern: the electrocardiogram showed ST-segment elevation in the lower part of the heart. In a typical scenario, this finding would trigger an immediate emergency response, likely involving a catheterization procedure to inspect the new grafts for blockages.

The medical team, however, paused to look at the full picture of the patient's condition. Unlike a patient having a heart attack, this man felt completely fine. He had no chest pain, his blood pressure was stable, and he did not require any extra medication to support his heart's pumping action. To investigate further, the doctors performed an ultrasound of the heart, which showed that the main pumping chamber was working at a normal strength and that there were no signs of the muscle being damaged or struggling in specific areas. They also checked the levels of troponin, a protein released into the blood when heart muscle cells are injured. While the level was slightly elevated, as is common after heart surgery, it was already on a steady decline, dropping from 0.9 nanograms per milliliter on the first day to 0.3 nanograms per milliliter by the third day. If the patient were suffering from an active heart attack or a blocked graft, these numbers would typically continue to rise or stay high.

In addition to the heart-specific tests, the doctors looked at markers of general inflammation in the body. They found that the patient's C-reactive protein was extremely high at 120 milligrams per liter, and his erythrocyte sedimentation rate was also significantly elevated at 68 millimeters per hour. These high numbers pointed strongly toward a widespread inflammatory response rather than a localized blockage of blood flow. The combination of a stable patient, a heart that was pumping normally, a declining trend in injury markers, and a surge in inflammatory signals suggested that the heart was not starving for oxygen. Instead, the evidence pointed to a condition known as post-pericardiotomy pericarditis. This is an inflammation of the sac surrounding the heart, which is a known and common reaction to the surgical trauma of opening the chest. This inflammation can irritate the heart's surface and cause the same electrical changes on a monitor that a blocked artery would produce.

Given this evidence, the team made a calculated decision to avoid an invasive angiogram, a procedure that involves threading a tube into the arteries to take pictures. For a patient with immune thrombocytopenia, even a stabilized one, an invasive procedure carries a heightened risk of bleeding. Since the clinical signs did not support a diagnosis of a blocked graft, the potential harm of the procedure outweighed the benefit. Instead, the team chose a conservative approach. They treated the patient with medications to reduce inflammation and monitored him closely with repeated heart rhythm tests and ultrasounds. They also carefully managed his blood thinners to protect the new grafts without causing bleeding. The strategy worked. By the third day after surgery, the abnormal ST-segment elevation had completely disappeared from the electrocardiogram. The patient remained stable, experienced no further complications, and was discharged a week after the operation. At a follow-up one month later, he was doing well with no return of symptoms or heart rhythm issues.

This case highlights a critical lesson for medical care: not every alarming signal on a heart monitor after surgery means a catastrophe. While the standard response to ST-segment elevation is often to assume the worst and intervene immediately, this report shows that in carefully selected patients who are stable and show signs of inflammation rather than muscle damage, a wait-and-see approach can be the safer and more correct choice. The presence of a blood disorder like immune thrombocytopenia and the use of drugs like romiplostim add layers of risk that make the decision to avoid invasive procedures even more significant. The doctors did not find a new disease or prove that the drug caused the heart changes; rather, they demonstrated how to distinguish between a true emergency and a temporary, non-dangerous reaction by looking at the whole patient. By integrating the patient's symptoms, the behavior of heart injury markers, and the signs of inflammation, the team successfully navigated a complex situation without subjecting the patient to unnecessary risks. The findings suggest that in similar cases, where a patient is stable and the heart function is preserved, the diagnosis of post-pericardiotomy pericarditis should be considered seriously before rushing to invasive testing.

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