Catastrophic multisystem arterial thromboembolism masked by acute ST-elevation myocardial infarction and cardiogenic shock in a rheumatic mitral stenosis patient: a case report

Abstract

Background

Severe rheumatic mitral stenosis with atrial fibrillation creates a highly thrombogenic left atrial substrate, particularly when anticoagulation is inadequate. Coronary embolism may present as ST-elevation myocardial infarction (STEMI) and can mask simultaneous systemic arterial embolization.

Case summary

A 60-year-old woman with severe rheumatic mitral stenosis, marked left atrial enlargement, atrial fibrillation, and irregular anticoagulation presented with STEMI complicated by cardiogenic shock. Coronary angiography revealed thrombotic occlusion of multiple distal coronary branches without significant underlying atherosclerosis, consistent with coronary thromboembolism. Manual aspiration thrombectomy restored Thrombolysis in Myocardial Infarction grade 3 flow. Despite partial haemodynamic stabilization, the patient developed persistent vasopressor dependence, anuria, severe metabolic acidosis, and progressive bilateral lower-limb ischaemia. Computed tomography angiography subsequently demonstrated multisystem arterial thromboembolism involving the superior mesenteric artery, abdominal aorta, bilateral iliac arteries, splenic artery, and bilateral renal arteries. The patient died from refractory multiorgan failure.

Discussion

This case illustrates that, in advanced rheumatic mitral stenosis and atrial fibrillation with inadequate anticoagulation, STEMI may be only one manifestation of a systemic embolic storm. Distal multivessel coronary occlusions without atherosclerosis, persistent metabolic deterioration after coronary reperfusion, and limb or visceral ischaemia should prompt early systemic vascular evaluation when clinically feasible.

Learning points.

• In rheumatic mitral stenosis with atrial fibrillation, inadequate vitamin K antagonist anticoagulation may cause coronary embolism without plaque rupture.

• ST-elevation myocardial infarction may represent the first visible sign of a broader systemic arterial embolic event.

• Persistent shock, acidosis, anuria, or peripheral/visceral ischaemia after coronary reperfusion should prompt urgent systemic vascular imaging.

Introduction

Rheumatic mitral stenosis (MS) complicated by atrial fibrillation (AF) represents one of the highest-risk clinical contexts for systemic arterial thromboembolism because valve obstruction, marked left atrial enlargement, and atrial mechanical dysfunction promote blood stasis and thrombus formation.¹ Current AF guidance recognizes moderate-to-severe MS as a setting in which vitamin K antagonist (VKA) anticoagulation remains the standard approach, and direct oral anticoagulants should generally be avoided.² While ischaemic stroke is the most recognized complication, extracerebral embolic events—including coronary, mesenteric, renal, and peripheral arterial embolization—remain underdiagnosed and are associated with substantial morbidity and mortality.³ Coronary thromboembolism is an important non-atherosclerotic mechanism of acute myocardial infarction, accounting for ∼3%–13% of cases, and is strongly associated with AF.⁴ Patients with AF-related coronary thromboembolism are more frequently women, older, and more likely to present with cardiogenic shock.⁵ In patients presenting with ST-elevation myocardial infarction (STEMI) complicated by cardiogenic shock, diagnostic attention is often narrowly focused on coronary reperfusion and haemodynamic stabilization. This approach, while lifesaving, may inadvertently obscure concomitant systemic embolization, resulting in delayed diagnosis and fatal outcomes. This report describes catastrophic multisystem arterial thromboembolism in advanced rheumatic MS with inadequate anticoagulation, where lateral STEMI represented one component of a much broader embolic event.

Summary figure

Case presentation

Timeline

Time	Event
Day 0–18:30	Sudden chest pain and dyspnoea after dinner
Day 0–20:00	Admission to regional hospital in cardiogenic shock; intubation, mechanical ventilation, and vasopressor/inotropic support
Day 0–22:30	Transfer to tertiary centre after initial stabilization and referral for emergent coronary angiography
Day 0–23:10	Coronary angiography showed distal LAD, distal LCx, and OM thrombotic occlusions without significant atherosclerosis; aspiration thrombectomy restored TIMI 3 flow
Day 1–0:00	Transfer to CICU. Persistent vasopressor dependence, anuria, metabolic acidosis, and progressive bilateral lower-limb ischaemia
Day 1–6:00	Continuous renal replacement therapy
Day 1–10:30	Computed tomography angiography revealed multisystem arterial embolization
Day 2–14:00	Death due to refractory multiorgan failure

A 60-year-old woman with a history of ischaemic stroke and rheumatic MS treated with percutaneous mitral balloon valvotomy 20 years earlier presented with acute chest pain and severe dyspnoea. She had not attended regular cardiology follow-up. The patient had been prescribed acenocoumarol, an oral VKA, with a target international normalized ratio (INR) of 2.0–3.0, but reported intermittent use for ∼3 months. The most recent INR, recorded 5 months ago, was 2.16, but the admission INR was only 1.43, indicating subtherapeutic anticoagulation at presentation. Following dinner, she developed sudden left-sided chest pain with rapidly progressive dyspnoea and impaired consciousness. About 1 h later, she was admitted to a regional hospital in cardiogenic shock, requiring intubation, mechanical ventilation, and high-dose inotropic and vasopressor support. Because of initial emergency stabilization and arrangement of inter-hospital transfer, the patient was admitted to our institution ∼4 h after symptom onset.

On arrival, she was sedated and mechanically ventilated, with haemodynamics dependent on dobutamine and norepinephrine. Electrocardiography demonstrated a junctional rhythm with ST-segment elevation in leads I, aVL, and V5–V6 (Figure 1). Transthoracic echocardiography (TTE) showed severe left atrial enlargement, global left ventricular hypokinesia with severely reduced systolic function, critical calcific mitral stenosis, and severe pulmonary hypertension. Quantitative echocardiographic parameters were a mitral valve area of 0.96 cm² by planimetry, a mean transmitral gradient of 7.0 mmHg at a heart rate of 65 beats/min, an estimated pulmonary artery systolic pressure of 84 mmHg, and a left atrial volume index of 116 mL/m². Left atrial thrombus was not visible, and the left atrial appendage was not adequately assessed by TTE, but transoesophageal echocardiography was not performed due to haemodynamic instability and urgent need for reperfusion. Laboratory testing revealed markedly elevated high-sensitivity troponin T (>10 000 ng/L), acute kidney injury, and severe hepatic dysfunction consistent with systemic hypoperfusion.

Figure 1.

Twelve-lead electrocardiogram at admission showing junctional rhythm with ST-segment elevation in leads I, aVL, and V5–V6, consistent with acute lateral wall myocardial infarction.

A diagnosis of lateral STEMI complicated by cardiogenic shock was made, and emergent coronary angiography was performed, with a plan to insert an intra-aortic balloon pump (IABP) if haemodynamic worsened during the procedure. Angiography revealed complete thrombotic occlusion of the distal left anterior descending artery (LAD), distal left circumflex artery (LCx), and obtuse marginal branch (OM), without significant atherosclerotic disease (Figure 2A). Manual aspiration thrombectomy restored Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow (Figure 2B, C). The patient was then transferred to the cardiac intensive care unit (CICU). Despite partial haemodynamic stabilization without the need for IABP support, the patient remained vasopressor-dependent and developed refractory anuria and metabolic acidosis. Continuous renal replacement therapy was initiated 6 h after coronary intervention. Progressive bilateral lower-limb cyanosis was initially attributed to vasopressor-induced vasoconstriction and low-flow shock. However, the combination of persistent severe acidosis, anuria, bilateral limb ischaemia, and non-atherosclerotic distal coronary thrombi raised concern for systemic embolization, prompting computed tomography angiography.

Figure 2.

(A) Baseline invasive coronary angiogram, illustrating complete thrombotic occlusion of the distal left anterior descending artery, distal left circumflex artery, and obtuse marginal branch (arrows), without significant atherosclerotic disease. (B, C) Coronary angiography demonstrated Thrombolysis in Myocardial Infarction grade 3 flow following aspiration thrombectomy. (D) Thrombi aspirated from the patient’s coronary arteries.

Computed tomography angiography, performed 12 h after transfer to the CICU, confirmed extensive arterial embolization. The affected territories included the superior mesenteric artery, near-complete thromboembolism of the abdominal aorta at the level of the inferior mesenteric artery with extension into both common iliac arteries, splenic artery occlusion, and multifocal bilateral renal infarctions (Figure 3). The patient developed refractory metabolic acidosis and multiorgan failure and died despite maximal supportive therapy.

Figure 3.

(A) Computed tomography angiography showed near-complete thromboembolism of the abdominal aorta and both common iliac arteries (arrowhead). (B) Thromboembolism affecting the superior mesenteric artery (arrowhead). (C) Multifocal bilateral renal infarctions (arrowheads).

Discussion

This case highlights that, in advanced rheumatic MS with marked left atrial enlargement and inadequate anticoagulation, STEMI may represent the first apparent manifestation of a systemic embolic storm rather than the primary disease process. The central pathophysiological driver was likely a highly thrombogenic left atrium resulting from critical rheumatic MS, atrial enlargement, AF, impaired left atrial emptying, and subtherapeutic anticoagulation. Although AF likely contributed to thrombus formation, the extensive embolic burden is better explained by advanced rheumatic valvular disease with severe atrial stasis. In this setting, coronary embolism was one component of widespread systemic arterial thromboembolism involving the abdominal aorta, mesenteric, splenic, renal, and bilateral iliac arteries.

Atrial fibrillation has historically been associated with ischaemic stroke; however, it is also correlated with both type-1 and type-2 myocardial infarction.⁶ Published series suggest that coronary thromboembolism accounts for ∼3%–13% of acute myocardial infarction and is frequently linked to AF.^4,5 Among STEMI patients with concomitant AF, coronary embolism may account for up to one-fifth of cases and is associated with higher rates of cardiogenic shock and early mortality.^5,7 The left anterior descending artery is commonly reported as the most frequent culprit vessel in coronary embolism, but emboli may affect any coronary territory.⁴ In the present case, simultaneous distal LAD, LCx, and OM occlusions without significant atherosclerosis were especially suggestive of an embolic rather than plaque-rupture mechanism.

In patients with atrial fibrillation, extracerebral systemic embolization remains an under-recognized but potentially fatal complication.⁸ The consequences are particularly severe when emboli affect the visceral circulation, for which mortality reached 45.5% in the ROCKET AF trial.⁹ Visceral embolic events have been reported in ∼1%–6% of patients with AF, most commonly affecting the splenic, renal, and mesenteric arterial territories.¹⁰

The case also illustrates a process failure that is common in acute cardiac care: diagnostic anchoring after apparently successful coronary reperfusion. Bilateral limb cyanosis, anuria, and metabolic acidosis were initially interpreted in the context of vasopressor therapy, low cardiac output, and multiorgan hypoperfusion. These explanations were plausible, but they became insufficient once TIMI 3 coronary flow had been restored and clinical deterioration persisted. Earlier recognition of the discordance between restored epicardial coronary flow and worsening systemic metabolic status may have prompted earlier systemic vascular imaging.

From a prevention perspective, this case reinforces the importance of guideline-concordant anticoagulation and longitudinal follow-up in rheumatic MS with AF. VKA therapy with regular INR monitoring remains the standard anticoagulant strategy for AF associated with moderate-to-severe rheumatic MS, whereas direct oral anticoagulants are not generally recommended in this population.^2,11 For patients with poor anticoagulation adherence, prevention should extend beyond prescription alone and include structured INR follow-up, targeted patient education, referral to an anticoagulation clinic, and timely reassessment for possible valve intervention.¹²

The practical message for interventional cardiologists and intensivists from this case is that coronary thromboembolism should not be managed only as an unusual STEMI pattern, especially in patients with MS and AF. Clinical clues that should raise suspicion for systemic embolization in this setting include (i) STEMI with distal multivessel thrombotic occlusions and little or no atherosclerosis; (ii) rheumatic MS, severe left atrial enlargement, AF, or subtherapeutic anticoagulation; and (iii) persistent shock, severe metabolic acidosis, multiorgan dysfunction, or limb ischaemia despite restored coronary flow. When feasible, early systemic vascular imaging should be considered once these features are present.

Conclusion

In rheumatic MS with AF and inadequate anticoagulation, STEMI may be a consequence of coronary embolism within a wider systemic arterial embolic event. Distal multivessel coronary occlusions without significant atherosclerosis should prompt immediate reassessment for a cardioembolic mechanism. If shock, anuria, metabolic acidosis, abdominal signs, or limb ischaemia persist after coronary reperfusion, clinicians should pursue early systemic vascular imaging when clinically feasible.

Lead author biography

Dr Tran Quoc Quy, MD, is a cardiologist working in the Cardiovascular Intensive Care Unit at 108 Central Military Hospital, Hanoi, Vietnam. His clinical expertise centres on the management of critically ill patients with acute coronary syndromes, coronary circulation disorders, acute and advanced heart failure, hypertensive emergencies, myocardial diseases, and stroke. He has extensive experience in inpatient care and advanced echocardiography to guide haemodynamic assessment and decision-making in the intensive care setting. Dr Quy is actively involved in clinical research and peer-reviewed publications.

Author contributions

Quy Quoc Tran (Conceptualization, Visualization, Writing—original draft [lead]), Duc Viet Dang (Methodology, Supervision, Writing—review & editing [supporting]), and Chien Van Do (Investigation, Supervision [lead], Writing—original draft [equal])

Consent: The authors confirm that written consent has been obtained from the patient for the submission and publication of this case report, including images and associated tests, in accordance with the Committee on Publication Ethics (COPE) guidance.

Funding

None declared.

Data availability

The data underlying this article will be shared on reasonable request to the corresponding author, subject to institutional and privacy requirements.