ABSTRACT
Delayed STEMI presentation can cause extensive myocardial necrosis, left ventricular thrombus, cardiogenic shock, and progression to end‐stage heart failure despite reperfusion. Early recognition and timely transfer to specialized shock centers are critical. In refractory cases, advanced mechanical circulatory support (VA‐ECMO with Impella) may serve as a bridge to life‐saving heart transplantation.
1. Introduction
ST‐elevation myocardial infarction (STEMI) is a life‐threatening emergency condition caused by the complete coronary artery blockage, accounting for 25%–40% of myocardial infarctions worldwide, with higher incidence in low‐ and middle‐income countries [1]. Prompt recognition and timely reperfusion, either with thrombolytic therapy or percutaneous coronary intervention (PCI), are fundamental to the effective management of ST‐elevation myocardial infarction [2, 3]. Current guidelines recommend achieving reperfusion within 90–120 min of first medical contact in STEMI to optimize outcomes [4]. When these interventions are delayed, the resulting myocardial damage can lead to devastating complications including arrhythmias, irreversible left ventricular dysfunction, ventricular thrombi, cardiogenic shock, and progression to end‐stage heart failure [5, 6]. Despite advances in pharmacologic and mechanical interventions, outcomes remain poor in patients who present late in the course of infarction [7].
Early revascularization significantly improves survival and cardiac function, whereas also enhancing post‐resuscitation hemodynamic stability, 24‐h survival, and neurological outcomes [8], missed or delayed presentations continue to challenge healthcare systems, particularly in resource‐limited or non‐PCI‐capable settings [9]. Sometimes in rare but life‐threatening cases of ST‐elevation myocardial infarction (STEMI), especially when patients present late and develop severe complications from prolonged ischemia, even aggressive medical therapy and advanced mechanical circulatory support may fail to restore adequate heart function, making heart transplantation the only remaining life saving option [10].
We present a compelling case of a patient who experienced a delayed presentation of anterior STEMI and subsequently developed refractory cardiogenic shock and end‐stage heart failure. Despite optimal medical therapy and the use of multiple mechanical circulatory support modalities including venoarterial extracorporeal membrane oxygenation (VA‐ECMO) and Impella 5.5, the patient ultimately required orthotopic heart transplantation. Recent studies have shown that outcomes in cardiogenic shock are improved when patients are managed at specialized cardiogenic shock centers with high patient volumes, 24/7 PCI capability, access to mechanical circulatory support, and multidisciplinary expertise. Early transfer to such centers is considered a key system‐level factor in the management of refractory cardiogenic shock [11]. This case underscores the life‐altering consequences of delayed STEMI treatment and the crucial role of mechanical circulatory support as a bridge to transplantation in patients with refractory cardiogenic shock [12].
2. Case Presentation
A 57‐year‐old white American male with no known prior cardiac history, but with a history of cannabis use, presented to a non–PCI‐capable emergency department with severe, active chest pain. He reported experiencing on and off chest pain and shortness of breath for the past 1 month. On arrival, his initial electrocardiogram (EKG) demonstrated antero‐septal ST‐segment elevations along with Q‐waves (Figure 1). Cardiac biomarkers were significantly elevated including high‐sensitivity troponins and B‐type natriuretic peptide (BNP) (Table 1). Given the new onset of persistent chest pain, the absence of contraindications to thrombolytic therapy, and the facility's lack of PCI capability, the patient was treated with tenecteplase (TNK). Transthoracic echocardiography was not performed prior to fibrinolysis due to the patient's classic ST‐elevation myocardial infarction presentation, significantly elevated cardiac biomarkers, and the need for urgent reperfusion therapy in a non–PCI‐capable setting. At that time, the presence of left ventricular thrombus was unknown, and no clinical evidence of embolic or cerebrovascular complications occurred following fibrinolytic therapy. With subsequent improvement in symptoms, he was transferred to our facility for further evaluation and possible PCI.
FIGURE 1.
Pre‐lytic electrocardiogram (EKG) showing marked ST‐segment elevation in the anteroseptal leads (V1–V4) with the presence of pathological Q waves.
TABLE 1.
Cardiac biomarker profile demonstrating evidence of myocardial injury.
| Test | Result | Unit | Normal value |
|---|---|---|---|
| BNP | 231 | pg/mL | < 100 |
| Creatine kinase (total) | 245 | U/L | 22–198 |
| Troponin I | 0.51 | ng/mL | < 0.04 |
| Troponin high sensitivity | 79 | ng/L | < 14 |
On arrival at our center, the patient was doing well overall, with no chest pain, hemodynamically stable vital signs, and no signs of respiratory distress. However, his repeat EKG continued to show distant anterior ST‐segment elevations (Figure 2). A transthoracic echocardiogram was performed, which showed severely depressed systolic function with an ejection fraction (EF) of approximately 20%, along with akinesis of the apical anterior, anterior septal, and anterior lateral walls, and left ventricular apical thrombus (Figure 3). Due to the persistent EKG abnormalities, the patient was taken to the catheterization lab for urgent coronary angiography, which revealed severe obstructive stenosis in the mid‐left anterior descending artery (LAD) with TIMI 1–2 distal flow (Figure 4A–C). Left heart catheterization confirmed the LAD lesion (Table 2). The lesion was successfully treated with plain old balloon angioplasty (POBA), followed by shockwave lithotripsy and placement of a drug‐eluting stent, which resulted in restoration of TIMI grade 3 flow through the mid‐LAD down the obstruction. Left ventricular end‐diastolic pressure (LVEDP) was not measured due to the presence of apical thrombus. Right heart catheterization showed elevated right ventricular pressure, pulmonary artery pressure, and pulmonary capillary wedge pressure, consistent with elevated filling pressures and cardiogenic shock (Table 3).
FIGURE 2.
Post‐lytic EKG showing distant anterior ST‐segment elevation.
FIGURE 3.
Transthoracic echocardiogram (apical two‐chamber view) demonstrating a left ventricular apical thrombus.
FIGURE 4.
(A–C) Coronary angiography demonstrating obstructive stenosis in the mid left anterior descending (LAD) artery with reduced antegrade flow (TIMI grade 1–2).
TABLE 2.
Left heart catheterization findings.
| Coronary vessel | Description | Additional notes |
|---|---|---|
| Left main (LM) | Large vessel, patent | No significant stenosis |
| Left anterior descending (LAD) | Patent proximally; 99% heavily calcified stenosis | Distal LAD small but patent, reaches AV groove |
| Diagonal 1 (D1) | Small | No major lesions reported |
| Diagonal 2 (D2) | Patent | No major lesions reported |
| Left circumflex (LCX) | Small, nondominant | No major lesions reported |
| Right coronary artery (RCA) | Large, dominant vessel; luminal irregularities mid and distal | No major lesions reported |
| Right posterior lateral (RPL) | Patent | Branch of RCA |
| Right posterior descending artery (RPDA) | Patent | Branch of RCA |
TABLE 3.
Right heart catheterization findings.
| Parameter | Value | Normal range |
|---|---|---|
| Right atrial (RA) pressure | 7 mmHg | 2–8 mmHg |
| Right ventricular (RV) pressure | 53/5 mmHg |
Systolic 15–30 mmHg Diastolic 2–8 mmHg |
| Pulmonary artery (PA) pressure | 50/29 mmHg (mean 37) |
Systolic 15–30 mmHg Diastolic 4–12 mmHg Mean 9–18 mmHg |
| Pulmonary artery wedge pressure (PAWP) | 24 mmHg | 6–12 mmHg |
| Arterial oxygen saturation | 94% | 95%–100% |
| Pulmonary artery saturation (SvO2) | 60% | 60%–80% |
| Cardiac output (Fick method) | 3.9 L/min | 4–8 L/min |
| Cardiac index (Fick method) | 2.1 L/min/m2 | 2.5–4.0 L/min/m2 |
| Cardiac output (thermodilution) | 2.8 L/min | 4–8 L/min |
| Cardiac index (thermodilution) | 1.4 L/min/m2 | 2.5–4.0 L/min/m2 |
Putting these findings together, the patient was diagnosed with a late‐presenting anterior wall ST‐elevation myocardial infarction (STEMI) complicated by severely reduced left ventricular systolic function, apical thrombus, and cardiogenic shock. Although the post‐PCI electrocardiogram (EKG) showed normalization of ST segments, the patient subsequently developed progressive hypotension and tachycardia, consistent with low‐output heart failure due to a marked reduction in ejection fraction by 20%. The patient was initially started on dobutamine for inotropic support, but due to worsening tachycardia, he was transitioned to milrinone to improve hemodynamic tolerance. For anticoagulation of the apical thrombus, he was started on an intravenous heparin drip and later transitioned to Eliquis (apixaban). Intravenous furosemide (Lasix) 40 mg twice daily was given for volume management. Despite being tachycardic and hypotensive, the patient remained electrically stable and did not require oxygen therapy. Mechanical circulatory support with Impella was considered but deferred due to the presence of apical thrombus, which poses a contraindication to device placement. The heart failure team was consulted, and after discussion, it was determined that no further escalation of care was necessary at that time.
Guideline‐directed medical therapy (GDMT) for heart failure was initiated. The patient was started on metoprolol for rate control, beginning at a low dose with plans to increase dose based on clinical tolerance. On the day of discharge, the patient had been on milrinone for 2 days and remained on GDMT plus metoprolol. He was discharged in a hemodynamically stable condition, with a blood pressure of 96/68 mmHg, no requirement for supplemental oxygen, and was provided with a LifeVest wearable defibrillator for arrhythmia protection. He was instructed to follow up with the heart failure team within 1 week and to undergo a repeat echocardiogram in 3 months to assess for resolution of the apical thrombus. The patient was also advised to continue triple antithrombotic therapy for 1 month. After the initial month, it was decided to discontinue aspirin, and he was instructed to continue dual therapy with Plavix (clopidogrel) and Eliquis (apixaban) thereafter.
3. Second Visit After Hospital Discharge
One week after discharge, the patient presented again to the emergency department with severe shortness of breath, cold sweats, profound fatigue, and dyspnea on exertion. He reported strict adherence to prescribed medications and stated he had been wearing the LifeVest consistently until that morning. He described a sudden worsening of his symptoms, stating he became so short of breath that he felt unable to complete a breath and had to gasp for air. Additionally, he reported orthopnea and bendopnea, but denied lower extremity edema. He also denied fever, chills, rigors, rhinorrhea, cough, or chest pain. All the labs including the CBC were normal. An electrocardiogram (EKG) demonstrated sinus tachycardia (Figure 5). However, lactate was markedly elevated at 13.8 mmol/L, and both troponin and BNP levels were elevated, raising concern for worsening cardiac function. The patient was admitted to the intensive care unit (ICU) after consultation with the cardiology service.
FIGURE 5.
ECG demonstrating sinus tachycardia.
On physical examination, his blood pressure was 92/63 mmHg, heart rate 98 bpm, and respiratory rate 18 breaths/min. He initially started on BIPAP for respiratory support and levosimendan but was later switched to dobutamine due to hemodynamic considerations. A chest X‐ray showed bilateral pulmonary infiltrates consistent with pulmonary edema (Figure 6). Because of ongoing shock and respiratory failure, the patient underwent right heart catheterization, which revealed severely elevated right atrial pressure, along with markedly elevated right ventricular and pulmonary artery pressures, and a pulmonary capillary wedge pressure (PCWP) of 30 mmHg (Table 4). These hemodynamic findings were indicative of refractory cardiogenic shock with biventricular failure, most likely secondary to decompensated end‐stage heart failure. Despite initiation of aggressive therapy, including vasoactive inotropic agents and intravenous diuretics, the patient's condition continued to worsen, necessitating consideration of advanced mechanical circulatory support. As a result, venoarterial extracorporeal membrane oxygenation (VA‐ECMO) was initiated, along with placement of an Impella 5.5 device for left ventricular unloading. The case was subsequently reviewed by the heart transplant committee, and after discussion, the patient's family agreed to proceed with heart transplantation. The patient remained on VA‐ECMO, Impella support, heparin anticoagulation, and vasoactive agents as a bridge to transplant.
FIGURE 6.
Chest X‐ray showing bilateral pulmonary infiltrates.
TABLE 4.
Hemodynamics from right heart catheterization consistent with decompensated end‐stage heart failure.
| Parameter | Value | Normal range |
|---|---|---|
| Right atrial (RA) pressure | 25 mmHg | 2–8 mmHg |
| Right ventricular (RV) pressure | 50/20 mmHg |
Systolic 15–30 mmHg Diastolic 2–8 mmHg |
| Pulmonary artery (PA) pressure | 61/42 mmHg (mean 46) |
Systolic 15–30 mmHg Diastolic 4–12 mmHg Mean 9–18 mmHg |
| Pulmonary artery wedge pressure (PAWP) | 30 mmHg | 6–12 mmHg |
| Aortic saturation (arterial oxygen saturation) | 91% | 95%–100% |
| Pulmonary artery saturation (SvO2) | 26% | 60%–80% |
| Cardiac output | 2.09 L/min | 4–8 L/min |
| Cardiac index | 1.33 L/min/m2 | 2.5–4.0 L/min/m2 |
The patient underwent a successful orthotopic heart transplant under the supervision of the transplant team. Postoperatively, he was initiated on an immunosuppressive regimen consisting of prednisone 20 mg daily, mycophenolate mofetil 1000 mg twice daily, and tacrolimus 5 mg daily. He continues to follow up regularly with the heart transplant team for ongoing postoperative care and long‐term management.
4. Discussion
In ST‐elevation myocardial infarction (STEMI), delayed presentation remains a major challenge, particularly in resource‐limited settings or regions without timely access to percutaneous coronary intervention (PCI). Prolonged ischemic time is associated with extensive myocardial necrosis and adverse sequelae including intracardiac thrombus formation, cardiogenic shock, and progression to end‐stage heart failure. In non–PCI‐capable settings, time‐sensitive fibrinolysis for STEMI remains a guideline‐supported reperfusion strategy when classic clinical and electrocardiographic criteria are present. In our case, the urgency of reperfusion outweighed the feasibility of pre‐lysis imaging, and fibrinolytic therapy appropriately preceded echocardiography. Despite initial thrombolytic therapy and subsequent successful PCI, the patient's extensive anterior infarction, severely reduced left ventricular (LV) function, and development of apical thrombus were largely attributable to delayed presentation and seeking care.
Large anterior myocardial infarctions are well known to predispose patients to LV dysfunction and apical thrombus formation. In a serial echocardiographic study of 92 patients with first anterior myocardial infarction, Visser et al. [12] reported LV thrombus in 33% of cases, with persistent thrombus associated with worsening apical wall motion and declining global LV function. Similarly, in a large cohort of 1753 patients with first anterior MI, LV apical thrombus was identified in 5.6% and was associated with longer symptom‐to‐treatment delays, poorer post‐PCI flow, and lower ejection fraction [13]. These findings underscore the close relationship between infarct size, impaired ventricular mechanics, and thrombus formation.
Apical thrombus in the setting of severe LV dysfunction is a known complication of large anterior infarctions [14]. Following an acute myocardial infarction, left ventricular thrombi develop in accordance with Virchow's triad, which comprises three essential elements: hypercoagulability, endothelial damage, and blood stasis. All three elements are present and work together to provide a prothrombotic environment in a setting of large anterior infarctions with substantial left ventricular failure [15, 16, 17]. Systemic fibrinolytic therapy in the presence of left ventricular thrombus carries a potential risk of thrombus fragmentation and systemic embolization including ischemic stroke. However, in non–PCI‐capable settings, fibrinolysis remains a guideline‐supported reperfusion strategy when timely primary PCI is unavailable. In this case, the left ventricular apical thrombus was identified only after fibrinolysis had been administered, and the patient did not experience any clinical evidence of cerebrovascular embolic events. This highlights the challenging balance between urgent reperfusion and embolic risk in late‐presenting STEMI patients, particularly when advanced imaging is not immediately available.
A recent scoping review has highlighted that outcomes in cardiogenic shock are closely linked to institutional factors including higher case volumes, availability of advanced mechanical circulatory support, and dedicated cardiac intensive care units. These findings support early referral of patients with refractory shock to specialized cardiogenic shock centers capable of delivering advanced heart failure therapies including heart transplantation [11]. Despite initiation of anticoagulation and guideline‐directed medical therapy, the patient developed recurrent episodes of cardiogenic shock with progressive hemodynamic deterioration. Although inotropic agents are frequently required in this setting, current evidence does not demonstrate a clear mortality benefit of milrinone over dobutamine. Consequently, inotrope selection is guided by hemodynamic profile and tolerability rather than superiority. In our patient, worsening tachycardia on dobutamine prompted transition to milrinone; however, low‐output heart failure persisted [18, 19]. This clinical course illustrates the limited efficacy of inotropes alone in advanced ischemic cardiomyopathy and emphasizes the need for timely escalation to mechanical circulatory support (MCS). Furthermore, standard pharmacologic regimens may be unsafe or ineffective in cardiogenic shock due to altered drug pharmacokinetics in the context of impaired tissue perfusion, systemic inflammation, and multiorgan dysfunction [20].
In order to stabilize the patient and manage multiorgan dysfunction, mechanical circulatory support (MCS) with Veno‐arterial extracorporeal membrane oxygenation (VA‐ECMO) and Impella for LV unloading was essential. This method is in line with new approaches that use advanced MCS to treat refractory cardiogenic shock and pave the way for definitive treatment such as transplantation. VA‐ECMO increases LV pressure, LV size, and LV wall strain by supporting counterflow into the systemic circulation. The increase in left ventricular afterload caused by this retrograde aortic flow can paradoxically exacerbate myocardial oxygen consumption and delay cardiac recovery [21]. Durable left ventricular assist devices (LVADs), such as HeartMate 3, are established options for advanced heart failure, particularly in patients with predominantly left ventricular dysfunction and in the setting of donor organ scarcity. In this case, LVAD therapy was considered; however, the patient's rapidly progressive refractory cardiogenic shock, dependence on VA‐ECMO, and concern for inadequate end‐organ recovery limited the feasibility of durable device implantation. Consequently, urgent orthotopic heart transplantation was pursued as the definitive life‐saving strategy. This case highlights the complexity of selecting advanced heart failure therapies and underscores the need for individualized, multidisciplinary decision‐making when balancing LVAD therapy versus transplantation in critically ill patients.
On the other hand, even in the absence of LV ejection and a closed aortic valve, blood flows from the LV to the aorta because the Impella constantly drains the LV and sends the blood to the proximal aorta [22]. When Impella and VA‐ECMO are used together, the LV size, LV pressure, and LV wall tension all drop at the same time, increasing cardiac output [21]. By combining the two devices, a special hemodynamic environment is produced that optimizes their respective advantages while reducing their limitations.
The significance of early detection and reperfusion in STEMI to prevent the progression of end‐stage heart failure necessitating a transplant is highlighted by the present case. Additionally, it draws attention to how advanced MCS may help stabilize patients experiencing refractory cardiogenic shock so they can recover or transition to more effective treatments. Our patient's remarkable postoperative outcome shows that even in the setting of catastrophic ischemic myocardial injury, prompt escalation to advanced treatment, such as transplantation, can produce outstanding outcomes. Importantly, the success of a thrombolysis‐to‐transplant strategy likely depends not only on the initial reperfusion therapy but also on rapid referral to specialized centers capable of delivering advanced cardiogenic shock care. In this regard, recent evidence suggests that outcomes are improved in dedicated cardiogenic shock centers characterized by high patient volumes, continuous PCI availability, structured hub‐and‐spoke systems, and access to advanced heart failure therapies including LVAD and transplant programs [22].
5. Conclusion
Delayed presentation of STEMI can lead to extensive myocardial injury, cardiogenic shock, and progression to end‐stage heart failure despite timely fibrinolysis and revascularization. In non–PCI‐capable settings, emergency fibrinolysis may be required based on classical clinical and electrocardiographic findings, even when pre‐treatment echocardiography is not feasible. This case illustrates the limited efficacy of inotropic therapy alone and the need for individualized hemodynamic management. Advanced mechanical circulatory support with VA‐ECMO and Impella was essential for stabilization in refractory shock. Although durable LVAD therapy represents an important alternative in selected patients, urgent heart transplantation may be required in cases of rapidly progressive shock and limited recovery potential. The patient's successful outcome following transplant highlights the importance of early recognition, rapid escalation of care, and the availability of advanced therapies. This case emphasizes the need for timely reperfusion and coordinated multidisciplinary management in complex STEMI cases.
Author Contributions
Syed Rafay Hussain Zaidi: conceptualization. Muhammad Sheraz Hameed: data curation, writing – original draft. Muhammad Ahsan: data curation, formal analysis. Hamza Ishfaq: investigation, methodology, software. Ali Iqbal: project administration, visualization. Azka Mirza: investigation, writing – original draft. Sadia Rekhum: investigation, writing – original draft. Muhammad Sohaib Alvi: supervision, validation, writing – review and editing. Muhammad Usama Naveed: project administration, resources, software.
Funding
The authors have nothing to report.
Ethics Statement
Written informed consent was obtained from the patient to publish the material.
Consent
Written informed consent was obtained from the patient's legal guardian for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor‐in‐Chief of this journal.
Conflicts of Interest
The authors declare no conflicts of interest.
Acknowledgments
The authors have nothing to report.
Data Availability Statement
Data will be provided on request by the corresponding author.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
Data will be provided on request by the corresponding author.