Recurrent bilateral lower limb arterial embolism secondary to left ventricular thrombus in peripartum cardiomyopathy successfully treated with systemic streptokinase thrombolysis: a rare case report

Abstract

Background

Peripartum cardiomyopathy (PPCM) is an uncommon but potentially life-threatening form of heart failure occurring toward the end of pregnancy or during the months following delivery in women without pre-existing heart disease. Left ventricular systolic dysfunction predisposes patients to intracardiac thrombus formation and systemic thromboembolic complications, which are associated with significant morbidity and mortality.

Case presentation

A 35-year-old multiparous woman presented shortly after spontaneous vaginal delivery of an intrauterine fetal demise with acute right lower-limb ischemia and heart failure. Transthoracic echocardiography demonstrated severe left ventricular systolic dysfunction (LVEF approximately 35%), severe functional mitral regurgitation, pulmonary hypertension, and a large left ventricular thrombus. She underwent urgent Fogarty embolectomy followed by therapeutic anticoagulation with unfractionated heparin and warfarin. Despite therapeutic anticoagulation (INR 2.0 and activated partial thromboplastin time approximately 90 seconds), she developed recurrent bilateral acute lower-limb ischemia five days later. Because of profound hemodynamic instability and prohibitive surgical risk, systemic streptokinase thrombolysis was administered. Repeat echocardiography performed immediately after thrombolysis demonstrated complete resolution of the left ventricular thrombus. Follow-up echocardiography one week later showed significant recovery of left ventricular systolic function (LVEF 45–50%), improvement of mitral regurgitation to mild-to-moderate, and reduction in pulmonary artery systolic pressure.

Conclusion

This case highlights the importance of early recognition of thromboembolic complications in PPCM and demonstrates that systemic streptokinase thrombolysis may represent an effective life- and limb-saving therapeutic option in carefully selected patients when surgical or catheter-based interventions are not feasible.

Supplementary Information

The online version contains supplementary material available at https://doi.org/10.1186/s12872-026-06268-9.

Introduction

Peripartum cardiomyopathy (PPCM) is an idiopathic form of systolic heart failure that develops toward the end of pregnancy or within the months following delivery in women without previously recognized structural heart disease. It is characterized by left ventricular systolic dysfunction, typically with an ejection fraction below 45%, after exclusion of other identifiable causes of cardiomyopathy [1, 2].

Although PPCM remains relatively uncommon, it is associated with substantial maternal morbidity and mortality [3]. Several risk factors have been identified, including advanced maternal age, hypertensive disorders of pregnancy, multiple gestation, and African ancestry [4, 5].

Pregnancy itself is characterized by a physiological hypercoagulable state. When combined with severe left ventricular dysfunction and intracardiac blood stasis, patients with PPCM become particularly susceptible to left ventricular thrombus formation and systemic thromboembolic complications [6, 7]. Systemic arterial embolization remains an uncommon but potentially catastrophic manifestation, capable of causing acute limb ischemia, stroke, mesenteric ischemia, and other life-threatening complications.

Early diagnosis of PPCM is often challenging because its symptoms frequently overlap with the physiological changes of late pregnancy and the postpartum period, resulting in delayed recognition. Transthoracic echocardiography remains the cornerstone of diagnosis by demonstrating left ventricular systolic dysfunction and identifying intracardiac thrombi when present [1, 2, 7].

Herein, we report a rare case of recurrent bilateral lower-limb arterial embolism secondary to a large left ventricular thrombus complicating PPCM. Despite therapeutic anticoagulation following surgical embolectomy, the patient experienced recurrent extensive arterial embolization that was successfully treated with systemic streptokinase thrombolysis, resulting in rapid thrombus resolution and significant recovery of cardiac function.

Case presentation

A 35-year-old multiparous woman (G3P1 + 1) with no previous history of cardiovascular disease, cardiomyopathy, valvular heart disease, or thromboembolic disorders was diagnosed with intrauterine fetal demise (IUFD) at 36 weeks of gestation. There was no previous history of heart failure symptoms before pregnancy. She subsequently underwent spontaneous vaginal delivery at a rural hospital.

Shortly after delivery, she developed sudden severe pain, coldness, and paralysis of the right lower limb, followed by progressive dyspnea and hypoxemia, prompting transfer to the intensive care unit.

On admission, she was hypotensive (90/50 mmHg), tachycardic (130 beats/min), tachypneic (35 breaths/min), and hypoxic (SpO₂ 92% on room air). Physical examination revealed elevated jugular venous pressure, a pansystolic murmur consistent with severe mitral regurgitation, bilateral basal pulmonary crackles, and absent right femoral, popliteal, and distal arterial pulses. The right lower limb was cold, cyanotic, and paralyzed, consistent with acute limb ischemia. Electrocardiography demonstrated sinus tachycardia with ST-segment depression in leads I, aVL, V5, and V6. Chest radiography showed cardiomegaly with pulmonary vascular congestion.

Transthoracic echocardiography demonstrated severe left ventricular systolic dysfunction with an estimated left ventricular ejection fraction (LVEF) of approximately 35%, a large mobile left ventricular thrombus measuring approximately 3 × 2 cm, severe left atrial dilatation, severe functional mitral regurgitation, moderate tricuspid regurgitation, and pulmonary hypertension (estimated systolic pulmonary artery pressure 50–55 mmHg) (Fig. 1).

Fig. 1.

(a) Lower extremities before treatment, demonstrating livedo reticularis and clinical signs of acute limb ischemia. b Restoration of skin color and Improvement of peripheral perfusion following streptokinase therapy

Contrast-enhanced computed tomography angiography confirmed extensive thrombotic occlusion involving the external iliac artery, common femoral artery, superficial femoral artery, popliteal artery, and proximal tibial arteries of the right lower extremity (Figs. 2 and 3).

Fig. 2.

Contrast-enhanced CT angiography of the lower extremity demonstrating a filling defect with complete non-opacification of the external iliac artery throughout its course, extending to the level of the common femoral artery bifurcation. Non-opacification is also noted In the superficial femoral artery, popliteal artery, and the proximal segments of the anterior tibial and peroneal arteries. Distal runoff vessels remain opacified

Fig. 3.

Axial contrast-enhanced CT scan of the chest demonstrating a large hypodense thrombus within the left ventricular cavity

Bilateral lower-extremity venous duplex ultrasonography demonstrated no evidence of deep or superficial venous thrombosis. In addition, CT angiography showed no radiological findings suggestive of May-Thurner syndrome.

Laboratory investigations for autoimmune and inherited thrombophilia, including antinuclear antibodies (ANA), perinuclear antineutrophil cytoplasmic antibodies (p-ANCA), cytoplasmic antineutrophil cytoplasmic antibodies (c-ANCA), and antiphospholipid antibodies, were negative.

A diagnosis of peripartum cardiomyopathy complicated by left ventricular thrombus and systemic arterial embolization was established.

Emergency Fogarty embolectomy of the right femoral artery was successfully performed, followed immediately by therapeutic anticoagulation with intravenous unfractionated heparin. Successful thrombus retrieval was achieved. Warfarin was subsequently initiated with overlap therapy until therapeutic anticoagulation was achieved.

The patient initially demonstrated marked clinical improvement, with restoration of right lower-limb perfusion and recovery of motor function.

However, five days later, despite anticoagulation within the therapeutic range (INR 2.0 and activated partial thromboplastin time approximately 90 s), she developed sudden recurrent bilateral acute lower-limb ischemia characterized by absent femoral and distal pulses, cyanosis, severe pain, and paralysis.

Because of profound hemodynamic instability, repeat CT angiography was not feasible. Instead, urgent bedside arterial duplex ultrasonography demonstrated bilateral femoral artery thrombosis extending into the iliac arteries, right popliteal artery thrombosis, and absence of arterial flow throughout both lower extremities.

Repeat transthoracic echocardiography performed immediately before thrombolytic therapy continued to demonstrate the presence of the left ventricular thrombus (Supplementary Video 1).To provide a clear overview of this complex clinical course, a detailed chronological timeline summarizing all major clinical events, diagnostics, and interventions is illustrated in (Table 1).

Table 1.

Timeline of the patient's clinical course

Given the patient’s critical clinical condition and the prohibitively high risk of repeat surgical intervention or catheter-directed thrombolysis, systemic thrombolysis with intravenous streptokinase (1.5 million IU administered over 60 min) was initiated.

Immediately following completion of streptokinase infusion, repeat transthoracic echocardiography demonstrated complete disappearance of the left ventricular thrombus (Supplementary Video 2). Simultaneously, marked clinical improvement in lower-limb perfusion was observed.

Repeat arterial duplex ultrasonography demonstrated restoration of bilateral common femoral artery patency, with triphasic arterial flow throughout the entire arterial tree of the left lower extremity. Residual thrombotic occlusion persisted only within the right popliteal artery.

No major bleeding or hemorrhagic complications occurred during or after systemic thrombolytic therapy.

The patient remained on long-term anticoagulation together with guideline-directed medical therapy for heart failure. Anticoagulation was resumed after thrombolysis once bleeding risk was considered acceptable.

Follow-up transthoracic echocardiography performed one week later demonstrated significant recovery of left ventricular systolic function (LVEF 45–50%), improvement of mitral regurgitation from severe to mild-to-moderate, and reduction in pulmonary artery systolic pressure.

The patient was discharged home in stable clinical condition with significant cardiovascular and vascular improvement.

Discussion

Peripartum cardiomyopathy (PPCM) is an uncommon but potentially life-threatening disorder characterized by left ventricular systolic dysfunction developing during the last month of pregnancy or within the months following delivery in the absence of another identifiable cause of heart failure [1, 2]. Although recovery of ventricular function occurs in many patients, PPCM remains associated with substantial maternal morbidity and mortality, particularly when complicated by severe ventricular dysfunction and intracardiac thrombus formation.

Pregnancy and the puerperium are physiological hypercoagulable states characterized by increased concentrations of procoagulant factors, reduced fibrinolytic activity, and venous stasis. When combined with severe left ventricular systolic dysfunction, blood stasis within the dilated left ventricle markedly increases the risk of mural thrombus formation and subsequent systemic arterial embolization. Previous studies have reported left ventricular thrombus in approximately 10–17% of patients with PPCM, particularly in those with severe left ventricular dysfunction [6, 8–10].

Our patient demonstrated several recognized risk factors for thrombus formation, including severe left ventricular systolic dysfunction (LVEF approximately 35%), marked left ventricular dilatation, severe functional mitral regurgitation, and the postpartum hypercoagulable state. Despite prompt surgical embolectomy and therapeutic anticoagulation with intravenous unfractionated heparin and warfarin (INR 2.0; aPTT approximately 90 s), she developed recurrent bilateral acute lower-limb arterial embolization within five days, emphasizing the highly thrombogenic nature of PPCM in selected patients.

Systemic arterial embolization is considerably less common than venous thromboembolic complications in PPCM. Reported manifestations include ischemic stroke, mesenteric ischemia, renal infarction, coronary embolism, and acute limb ischemia. Recurrent bilateral lower-limb arterial embolization despite therapeutic anticoagulation remains exceptionally rare, with only a limited number of comparable cases reported in the literature [11–13].

Current international guidelines recommend therapeutic anticoagulation in patients with PPCM who have severe left ventricular dysfunction and documented intracardiac thrombus because of the substantial risk of systemic embolization. Nevertheless, evidence guiding the management of recurrent embolization despite adequate anticoagulation remains limited, and most recommendations rely on expert opinion and individual case reports rather than randomized clinical trials.

One of the most remarkable aspects of this case is the rapid and complete disappearance of the left ventricular thrombus immediately following systemic streptokinase thrombolysis, as documented by transthoracic echocardiography. The diagnosis was further supported by follow-up echocardiography one week later, which demonstrated substantial recovery of left ventricular systolic function (LVEF 45–50%), improvement of mitral regurgitation, and reduction in pulmonary artery systolic pressure, findings that are characteristic of early recovery in PPCM.

The choice of systemic streptokinase deserves particular discussion. Catheter-directed thrombolysis and repeat surgical embolectomy are established therapeutic options for acute limb ischemia; however, our patient presented with recurrent bilateral ischemia associated with profound hemodynamic instability, rendering transfer for endovascular intervention or repeat surgery clinically hazardous. Under these circumstances, immediate systemic thrombolysis represented the fastest available reperfusion strategy. Importantly, no major bleeding or hemorrhagic complications occurred despite recent delivery, suggesting that carefully selected postpartum patients may tolerate systemic thrombolysis when the anticipated benefits outweigh the potential risks [14].

To our knowledge, immediate echocardiographic documentation of complete left ventricular thrombus resolution following systemic streptokinase in PPCM has rarely been reported.

Only limited evidence exists regarding systemic thrombolysis for PPCM-associated arterial embolization. Consequently, our case contributes valuable clinical evidence supporting systemic thrombolysis as a potential rescue strategy in patients with extensive arterial thromboembolism when conventional surgical or catheter-based approaches are not feasible.

Recent advances in endovascular thrombectomy have expanded treatment options for patients with extensive thrombotic disease. Aimanan et al. recently described successful management of extensive inferior vena cava thrombosis using the ClotTriever and FlowTriever systems when inferior vena cava filter placement was not feasible. Although their report involved venous rather than arterial thrombosis, it illustrates the continuing evolution of mechanical thrombectomy techniques for patients with a high thrombus burden [15]. Nevertheless, in emergency settings characterized by rapidly progressive ischemia and hemodynamic instability, immediate systemic thrombolysis may remain the only readily available reperfusion strategy, as illustrated by the present case.

This case also highlights the importance of serial echocardiographic assessment in PPCM. Echocardiography not only established the diagnosis but also documented persistence of the left ventricular thrombus before thrombolysis, immediate thrombus resolution following treatment, and early recovery of ventricular function during follow-up. These sequential findings considerably strengthen the causal relationship between the intracardiac thrombus and the recurrent systemic embolic events.

Conclusion

This case illustrates an exceptionally rare presentation of recurrent bilateral lower-limb arterial embolization secondary to left ventricular thrombus complicating peripartum cardiomyopathy despite therapeutic anticoagulation. Systemic streptokinase thrombolysis resulted in rapid resolution of the intracardiac thrombus, successful limb reperfusion, and early recovery of left ventricular function without major bleeding complications. Our experience suggests that systemic thrombolysis may represent a life- and limb-saving therapeutic option in carefully selected patients with PPCM who develop recurrent extensive arterial embolization when surgical or catheter-based interventions are not feasible. Further studies are required to better define the optimal management strategy for this uncommon but potentially catastrophic clinical scenario.

Authors' contributions

OA provided scientific supervision and guided the clinical management. RI managed the patient’s treatment and co-wrote the original draft. MA co-wrote the original draft, prepared the manuscript, and served as the corresponding author. HH and ReA co-wrote the original draft. RaI critically reviewed and edited the manuscript. All authors read and approved the final manuscript.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Data availability

All data generated or analyzed during this study are included in this published article.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Written informed consent was obtained from the patient 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.

Competing interests

The authors declare no competing interests.