An autopsy case report of extensive intramyocardial hemorrhage complicated with acute myocardial infarction

Abstract

Hemorrhagic myocardial infarction (HMI) is a complication associated with percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI). We carried out a successful PCI for a 59-year old Japanese man presenting with chest pain due to AMI over 5 h. The onset to balloon time was 363 min. The next morning, he suffered cardiogenic shock, even with an auxiliary circulating device, which eventually resulted in death. An autopsy revealed extensive HMI. The necrotic myocardium showed not only coagulation necrosis but also contraction band necrosis which suggests myocardial injury due to late reperfusion. Although the intramyocardial hemorrhage was confined to the necrotic area, it was beyond the perfusion area of the culprit artery. Here, we describe a case of death with severe HMI. HMI can be a serious complication and worsen prognosis.

<Learning objective: The aim of primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) is to recanalize the infarct related artery and salvage the ischemic myocardium. However, late reperfusion sometimes leads to hemorrhagic myocardial infarction (HMI) as a result of myocardial injury. To avoid extensive HMI in AMI patients, primary PCI should be performed as soon as possible.>

Introduction

Hemorrhagic myocardial infarction (HMI) can be a catastrophic complication associated with acute myocardial infarction (AMI) [1]. We present a case of cardiogenic shock after reperfusion therapy of anterior AMI which resulted in death. An autopsy revealed extensive HMI spreading almost entirely around the left ventricle (LV).

Case report

A 59-year-old Japanese man who was treated with percutaneous coronary intervention (PCI) for unstable angina 10 years ago presented with chest pain which occurred while mountain climbing for the first time in a decade. He descended the mountain and walked into the emergency room of our hospital by himself. By this time, 5 h had passed since incident onset.

Physical examination revealed a blood pressure of 141/102 mmHg, a Levine II/VI apical systolic murmur, and coarse crackles at the lower field of the bilateral lung. A 12 lead electrocardiogram revealed sinus rhythm with a rate of 95 bpm, QS pattern with ST-segment elevation in leads I, aVL and V2–V6, and reciprocal change in leads II, III and aVF. Echocardiography revealed severe hypokinesis at the anterior wall of the LV, and mild mitral regurgitation. The LV ejection fraction (EF) was 35% (Fig. 1A and B). There was no significant accumulation of effusion.

Fig. 1.

Echocardiography and histological findings of the myocardium. Short axis view (A) and 2-chamber view (B) at admission showed severe hypokinesis at the anterior wall of the left ventricle (LV), and LV ejection fraction (EF) was 35%. Short axis view (C) and 2-chamber view (D) the next morning revealed LV hypertrophy (septal: 14 mm, posterior wall: 14 mm) and dysfunction. LV wall motion got diffuse severe hypokinesis, and LVEF decreased to 20%. Although an increase in pericardial effusion was also shown, the right ventricle had not collapsed. Appearance of the heart with myocardial hemorrhage is shown in (E). Gross pathology of short axis sections of the heart [(F) middle section of left ventricle, (G) from the base to the apex] revealed antero-septal and lateral hemorrhagic myocardial infarction. Intramyocardial hemorrhage with diffuse and confluent packed red blood cells spread between myocytes with coagulation necrosis, migratory neutrophils, and microvascular obstruction are shown in (H) (hematoxylin–eosin 400×). Contraction band necrosis [(I) (Azan 200×)] which suggests myocardial injury due to late reperfusion. The hemorrhagic area was confined to the necrotic area with denucleated myocardium [(J) (hematoxylin-eosin 200×)].

He was diagnosed with acute coronary syndrome. Acetylsalicylic acid (81 mg/day) had been prescribed. Prasugrel (20 mg) was loaded in the emergency room. An emergency coronary angiography revealed an in-stent total occlusion of the bare metal stent (Driver coronary stent 3.5 mm/24 mm, Medtronic, Minnesota, USA) implanted to the middle section of the left anterior descending artery (LAD) (Fig. 2A and B). We performed PCI with a drug-coated balloon (SeQuent Please 3.5 mm/20 mm, B. Braun Melsungen AG, Berlin, Germany) after plain old balloon angioplasty. The door to balloon time was 62 min. However, the onset to balloon time was 363 min. Inspection using an intravascular ultrasound catheter (Opticross, Boston Scientific, Natick, Massachusetts, USA) revealed neither a coronary artery dissection nor any stent mal-apposition (Fig. 2C). The final shot of the angiography showed thrombolysis in myocardial infarction (TIMI) flow grade 3, no dissection, and no other significant stenosis (Fig. 2D and E). The activated clotting time (ACT) was controlled by 250 s. He was hospitalized in an intensive care unit. The serum creatine phosphokinase-MB peaked at 1192 U/L and the electrocardiogram showed 70% ST-segment resolution 4 h after reperfusion (Fig. 3).

Fig. 2.

Coronary artery findings. Coronary angiography at diagnosis (A,B) showed an in-stent total occlusion of the bare metal stent implanted to the left anterior descending artery (LAD). There was no visible coronary artery dissection, either in the intravascular ultrasound catheter findings (C) or the final shot of angiography after revascularization (D,E) showing thrombolysis in myocardial infarction flow grade 3. Histological examination of the LAD [(F) (Elastica Van Gieson 40×)] revealed a microscopic coronary artery dissection limited to part of the stent segment. RAO: right anterior oblique, CAU: caudal, and CRA: cranial.

Fig. 3.

The time course of electrocardiogram and cardiac enzymes. WBC: white blood cell, CPK: creatine phosphokinase, APTT: activated partial thromboplastin time, GOT: glutamic-oxaloacetic transaminase, LDH: lactic acid dehydrogenase, and CRP: C-reactive protein.

The next morning, he went into cardiogenic shock. Echocardiography showed the LV wall was hypertrophic compared to the previous day. LV function was diffusely reduced, with an EF of 20%. Although an increased pericardial effusion was revealed, the right ventricle had not collapsed (Fig. 1C and D). Color flow imaging could not detect any flow between the LV cavity and the pericardial space. Despite the continuous intravenous infusion of catecholamines, SvO2 was decreased to 60%. With right cardiac catheterization, the cardiac index decreased to 1.2 L/min/m². We suspected circulation insufficiency due to the extensive intramyocardial hemorrhage and pericardial effusion. With intra-aortic balloon pumping (IABP) and venoarterial extracorporeal membranous oxygenation (VA ECMO), vital signs became stable. The ACT was controlled by 160–180 s. The electrocardiogram changed to a complete right bundle branch block, and the ST-segment in leads II, III and aVF gradually elevated (Fig. 3). We planned a recheck of coronary angiography after VA ECMO decannulation. However, on day 4, VA ECMO flow became unstable, and ultimately, the patient died.

An autopsy revealed the HMI spread almost entirely around the LV from the middle to the apex, excluding the posterior wall (Fig. 1E–G). Heart weight was 470 g, and the bloody effusion was 550 mL. Centripetal hypertrophy was confirmed. The necrotic area of the myocardium showed not only coagulation necrosis but also microvascular obstruction (MVO) and contraction band necrosis (Fig. 1H and I). Although the intramyocardial hemorrhage was confined to the necrotic area (Fig. 1J), it was beyond the perfusion area of the LAD. There were no vascular problems, with the exception of a microscopic coronary artery dissection limited to the stent segment of the LAD (Fig. 2F).

Discussion

PCI is the current standard and most effective treatment for patients with ST-segment elevation AMI [2]. The aim of PCI is to restore blood flow and salvage the ischemic myocardium. However, the recanalization of an infarct related artery sometimes leads to HMI, which is believed to be caused by reperfusion injury with the extravasation of red blood cells through damaged endothelial walls [3], [4]. We carried out PCI for the present case and marked, diffuse HMI occurred which was one of the major causes of cardiogenic shock.

Historically, intramyocardial hemorrhage has been thought of as a rare complication of AMI. However, with cardiac magnetic resonance (CMR), myocardial hemorrhage can easily be detected, and several studies have shown it occurs in up to one quarter of patients with AMI [5], [6]. Ganame et al. demonstrated that the presence of myocardial hemorrhage detected with CMR was related to a lager infarct size after reperfusion therapy for AMI [5]. In general, intramyocardial hemorrhage occurs in already damaged myocardium due to coronary artery reperfusion, and it rarely expands beyond the infarct area [7]. However, the possibility that increased interstitial pressure caused by severe intramyocardial hemorrhage could lead to the compression and obstruction of the microvasculature and invasion of the adjacent islands of viable myocardium cannot be dismissed [8], [9].In our case, MVO and HMI expanded beyond the perfusion area of the LAD, as demonstrated histologically. Delayed elevation of the ST-segment in leads II, III and aVF (Fig. 3) suggested the progression of HMI to the inferior wall. Mather AN et al. have shown that the presence of reperfusion hemorrhage is associated with not only infarct size but also a greater extent of MVO [6]. Marked diffuse intramyocardial hemorrhage might cause MVO and result in expansion of the infarct area.

Another cause of circulation insufficiency was the bloody effusion. Because an autopsy revealed no evidence of any type of cardiac rupture, we hypothesized that the effusion originated within the hemorrhagic myocardium. Although it may have contributed to the cardiac diastolic dysfunction, we did not perform percutaneous or surgical pericardial drainage because of the absence of right ventricle collapse and the high risk of complications.

A primary question is how we could have prevented HMI and cardiac death in this case. A guideline of European Society of Cardiology recommends primary PCI as the preferred reperfusion strategy in patients within 12 h of symptom onset [2]. Therefore, our case who was admitted 5 h after onset of chest pain was a candidate for primary PCI. However, experimental data have shown that the extent of intramyocardial hemorrhage increases with the time delay before coronary reperfusion [4].In our case, we considered the late reperfusion of 6 h after onset to be one of the factors contributing to the severe HMI. The contraction band necrosis revealed by autopsy suggested the myocardial injury due to late reperfusion. The time course of cardiac enzymes demonstrated the onset time accuracy (Fig. 3). Antiplatelet therapy and ACT control for this case were appropriate. PCI was carried out successfully. Although a coronary artery dissection due to balloon dilation was histologically found in a part of the stent segment, we do not believe this dissection caused the intramyocardial hemorrhage because of its microscopic size and limited nature. Even with IABP and VA ECMO, the patient’s circulation could not be maintained. Thus, it seems that this patient avoided HMI and could have been saved if PCI was performed at an earlier stage. Registry data showed that extensive time delays reduce the benefit of primary PCI for AMI with respect to mortality [10]. It is important to educate people they should present to a hospital as soon as possible following chest pain.

Conclusion

Here, we report a death from cardiogenic shock with severe HMI after primary PCI. Intramyocardial hemorrhage can be a serious complication of AMI and affect mortality.

Declaration of Competing Interest

All authors declare that there is no conflict of interest.