https://orcid.org/0000-0002-8701-9200
Abstract
Haemorrhage at the puncture site is a serious complication of percutaneous coronary intervention (PCI).
A 73-year-old man underwent transfemoral intervention because of stable angina pectoris. After a rotational atherectomy, an everolimus-eluting stent was implanted from the left main trunk to the proximal site of the left anterior descending (LAD) artery. We also recognized that myocardial bridging was significantly induced at the middle portion of the LAD, which was not evident before the PCI. We suspected puncture-related haemorrhage and immediately performed lower limb arteriography. As a result, contrast media extravasation was observed at the branch of the right inferior epigastric artery. Finally, we performed coil embolization into the left common femoral artery, and the extravasation successfully disappeared. Four months later, he underwent coronary angiography. There were no findings of myocardial bridging.
Myocardial bridging during a PCI procedure may indicate hypercontraction because of haemorrhage.
Myocardial bridging during percutaneous coronary intervention procedure may suggest hypercontraction because of haemorrhage.
Introduction
The haemorrhagic shock caused by intra-abdominal and retroperitoneal haemorrhages is a serious complication of percutaneous coronary intervention (PCI).1 Timely detection of puncture site–related bleeding is critical for patient management. However, identifying this type of bleeding can be challenging, particularly when there is no visible swelling at the puncture site. In this case report, we present a patient with intra-abdominal haemorrhage in whom the presence of prominent myocardial bridging provided a crucial clue in identifying the underlying cause of hypotension.
Summary figure
| Coronary angiography | A man in his 70s was admitted for coronary intervention. On coronary angiography, myocardial bridging in the middle of the left anterior descending (LAD) branch was unremarkable. |
| 3 h later | His coronary intervention was successful. After treatment, myocardial bridging in the middle of the LAD branch became apparent. |
| 3 h 10 min later | We suspected trouble with his right inguinal puncture site. |
| 3 h 5 min later | His haemoglobin level had dropped from 11 g/gL to 6 g/dL. |
| 3 h 30 min later | We noticed that his right epigastric artery was injured, so we performed coil embolization and obtained haemostasis. |
| 7 days later | He was discharged on his own. |
| 4 months later | On his coronary angiography, myocardial bridging in the middle of the LAD branch disappeared. |
| Coronary angiography | A man in his 70s was admitted for coronary intervention. On coronary angiography, myocardial bridging in the middle of the left anterior descending (LAD) branch was unremarkable. |
| 3 h later | His coronary intervention was successful. After treatment, myocardial bridging in the middle of the LAD branch became apparent. |
| 3 h 10 min later | We suspected trouble with his right inguinal puncture site. |
| 3 h 5 min later | His haemoglobin level had dropped from 11 g/gL to 6 g/dL. |
| 3 h 30 min later | We noticed that his right epigastric artery was injured, so we performed coil embolization and obtained haemostasis. |
| 7 days later | He was discharged on his own. |
| 4 months later | On his coronary angiography, myocardial bridging in the middle of the LAD branch disappeared. |
| Coronary angiography | A man in his 70s was admitted for coronary intervention. On coronary angiography, myocardial bridging in the middle of the left anterior descending (LAD) branch was unremarkable. |
| 3 h later | His coronary intervention was successful. After treatment, myocardial bridging in the middle of the LAD branch became apparent. |
| 3 h 10 min later | We suspected trouble with his right inguinal puncture site. |
| 3 h 5 min later | His haemoglobin level had dropped from 11 g/gL to 6 g/dL. |
| 3 h 30 min later | We noticed that his right epigastric artery was injured, so we performed coil embolization and obtained haemostasis. |
| 7 days later | He was discharged on his own. |
| 4 months later | On his coronary angiography, myocardial bridging in the middle of the LAD branch disappeared. |
| Coronary angiography | A man in his 70s was admitted for coronary intervention. On coronary angiography, myocardial bridging in the middle of the left anterior descending (LAD) branch was unremarkable. |
| 3 h later | His coronary intervention was successful. After treatment, myocardial bridging in the middle of the LAD branch became apparent. |
| 3 h 10 min later | We suspected trouble with his right inguinal puncture site. |
| 3 h 5 min later | His haemoglobin level had dropped from 11 g/gL to 6 g/dL. |
| 3 h 30 min later | We noticed that his right epigastric artery was injured, so we performed coil embolization and obtained haemostasis. |
| 7 days later | He was discharged on his own. |
| 4 months later | On his coronary angiography, myocardial bridging in the middle of the LAD branch disappeared. |
Case presentation
A 73-year-old man with stable angina pectoris was admitted to our hospital. He underwent coronary bypass surgery 5 years ago. However, all his grafts were occluded. Therefore, he was admitted to our hospital to undergo percutaneous coronary intervention for the proximal site of the left anterior descending (LAD) artery. His coronary risk factors were hypertension, an ex-smoker. His blood pressure was 134/80 mmHg, and his pulse rate was 72/min, regular. He had no evidence of jugular venous distension, no murmur in his lung or heart sounds, and no oedema of the lower legs. His echocardiographic findings showed a left ventricular ejection fraction of 59%, no apparent wall motion abnormalities, and no evidence of left ventricular hypertrophy. His coronary angiography revealed 75% stenosis of the left main trunk (LMT) and 90% stenosis of the LAD artery with calcification in the proximal site. Myocardial bridging was not evident when coronary angiography was undergone. We performed transfemoral intervention based on the reduced fractional flow reserve value (0.66). Under ultrasound guidance, a 7 Fr sheath was inserted into his right common femoral artery, and a 6 Fr sheath was inserted into his common femoral vein. An everolimus-eluting stent (Xience SkypointTM 3.5 × 12 mm) was implanted from the LMT to the proximal site of the LAD after a rotational atherectomy. During the stent implantation procedure, we noticed that his blood pressure decreased and his heart rate gradually increased. At that exact moment, we recognized that myocardial bridging had been significantly induced at the middle portion of the LAD, which was not evident before the intervention (Figure 1A–D, Supplementary material online, Video S1, S2). Although there was no swelling at the puncture site, we suspected puncture-related haemorrhage and immediately performed lower limb arteriography. As a result, contrast media extravasation was identified at the branch of the right inferior epigastric artery (Figure 1E). His haemoglobin level had abruptly dropped from 11.3 g/dL to 7.0 g/dL (normal range at our hospital: 13.5∼17.6 g/dL). After reversing the heparin with protamine, we continued manual compression for 30 min, but extravasation persisted. Therefore, we opted to perform interventional haemostasis via the left common femoral artery (4 Fr sheath). We used a shepherd hook to cross the bifurcation and selected the right inferior epigastric artery. After crossing the 0.016 in guidewire (Fathom-16TM) and subsequently the microcatheter (breakthrough 2.2/2.9 Fr), coil embolization was successfully performed using five INTERLOCKTM and two TARGET XLR (Figure 1F). He required a total of four units of red blood cell transfusion. Finally, he was discharged on the seventh day on his own.
Coronary angiography images of the patient. Coronary angiography images of the patient were taken 1 month ago ((A) diastolic phase and (B) systolic phase). The appearance of myocardial bridging can be seen ((C) the diastolic phase and (D) the systolic phase (white arrow)). (E) Extravasation of the right inferior epigastric artery. (F) Extravasation disappeared after coil embolization.
Four months later, he underwent chronic coronary angiography. There were no findings of in-stent restenosis. Furthermore, coronary angiography showed no evidence of myocardial bridging.
Discussion
In our case, the patient experienced haemorrhagic shock during the PCI, which resulted in myocardial bridging. We considered cardiogenic shock due to coronary perforation or cardiac tamponade as the primary differential rather than haemorrhagic shock because the patient’s blood pressure decreased during the percutaneous transluminal coronary rotational ablation procedure. However, there was no evidence of flow limitation or perforation, and there was no enlargement of the cardiac shadow suggestive of tamponade. On the other hand, myocardial bridging prompted us to consider a condition that causes cardiac hypercontraction. It was reported that computed tomographic angiography detected 58% of myocardial bridging and coronary angiography revealed dynamic compression in 13.3% of total patients.2 In some autopsy series, myocardial bridging occurs at a rate of up to 80%.3 Myocardial bridging is defined as the intramural course of a major epicardial coronary artery, and dynamic compression frequently occurred in the LAD. We must be aware of the presence of coronary arteries in the muscles.
Myocardial bridging is generally a benign condition. During the systolic phase, the myocardium compresses the coronary arteries. Because coronary artery blood flow is significant during the diastolic phase, this is rarely a problem. On the other hand, increased heart rate decreased diastolic perfusion, and increased contractility can cause coronary artery ischaemia. Myocardial bridging is classified into two types4: superficial and deep muscle types. The superficial type does not cause constriction of coronary flow during systole. However, the deep muscle type can compress the coronary artery, leading to reduced blood flow and potential myocardial ischaemia. Previous reports showed that transient myocardial bridging in the LAD can occur during the treatment of acute inferior myocardial infarction.5,6 This phenomenon is believed to be caused by myocardium hypercontraction in the LAD branch region in an attempt to compensate for an acute inferior wall myocardial infarction.
The case report highlights hypercontraction in the heart, a condition in which the heart muscle contracts excessively, possibly due to tachycardia and reduced afterload caused by severe bleeding. It may lead to myocardial bridging and become prominent during the PCI, indicating massive bleeding. The statement emphasizes the complex medical condition and its potential causes, as well as this phenomenon.
Lead author biography
Dr. Mio Aono is a young resident in cardiology.
Supplementary material
Supplementary material is available at European Heart Journal – Case Reports online.
Consent: The authors confirm that written consent for submission and publication of this case report including images and associated text has been obtained from the patient in line with the Committee on Publication Ethics (COPE) guidance.
Funding: None declared.
Data availability
The data underlying this article are available in the article and its online Supplementary material.
References
Author notes
Conflict of interest: None declared.
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