Refractory intracardiac thrombosis in hypertensive emergency: a case of recurrent multi-chamber thrombi with therapeutic implications

Introduction

Hypertensive emergency is characterized by acute elevations in systolic blood pressure (BP) exceeding 180 mmHg or diastolic BP above 120 mmHg, accompanied by new or progressive end-organ damage manifestations—including stroke, myocardial infarction, or heart failure (1). These crises affect approximately 2% of hypertensive populations (2) and carry grave prognostic implications, with 5-year mortality rates approaching 100% due to multi-system organ involvement primarily impacting neurological, cardiovascular, and renal systems (3,4). The underlying pathophysiology involves endothelial disruption triggering platelet aggregation, fibrin deposition, and arterial fibrinoid necrosis that collectively establish prothrombotic conditions (5). Although thrombotic complications in renal arteries, the aorta, and left ventricle (LV) have been documented in this setting (6-8), a medical literature search revealed no prior reports of recurrent intracardiac thrombi despite adequate anticoagulation. Herein, we report a rare case of a 27-year-old male with recurrent intracardiac thrombi due to uncontrolled hypertensive emergencies. The dramatic pattern of spontaneous thrombus resolution followed by aggressive recurrence underscores critical management implications.

Case presentation

A 27-year-old male presented to Affiliated Hospital of Shandong University of Traditional Chinese Medicine with severe headache, dizziness, exertional dyspnea, and grade 3 hypertension (220/180 mmHg) documented on admission. Detailed laboratory findings on admission are presented in Table 1. Despite a 5-year hypertension diagnosis, he had never maintained regular pharmacotherapy. During the preceding 3 months, he reported intermittent fever, peripheral edema, and progressive dyspnea upon minimal exertion.

Initial transthoracic echocardiography (TTE) revealed left atrial (LA) dilation (LA anteroposterior diameter: 56 mm), increased left ventricular end-diastolic diameter (LVEDD: 55 mm), and severely reduced left ventricular ejection fraction (LVEF) (38%) (Table 2). Notably, an 18 mm × 12 mm thrombus was visualized at the LV apex (Figure 1A). Biochemical markers confirmed myocardial injury and dysfunction with elevated cardiac troponin-T, N-terminal brain natriuretic peptide (NT-proBNP), and serum creatinine (Table 1). We initiated urgent heart failure management and antihypertensive therapy. Within 24 hours, his BP decreased to 170/105 mmHg with concurrent symptomatic improvement. Hospital treatment included warfarin anticoagulation combined with nifedipine, arotinolol, and furosemide. A second TTE performed 1 week later demonstrated significant LVEF recovery to 54% (Table 2) and complete thrombus resolution (Figure 1B).

Figure 1 Serial echocardiographic evolution of recurrent intracardiac thrombi in hypertensive emergency. (A) Initial presentation revealing 18 mm × 12 mm apical left ventricular thrombus (as indicated by the white arrow). (B) Complete thrombus resolution following 1-week anticoagulation and antihypertensive therapy. (C) Recurrence 10 months later demonstrating a new 21 mm × 18 mm thrombus at the middle-lower anterior wall of LV (as indicated by the white arrow). (D) Concurrent 20 mm × 18 mm thrombus in the posterior left atrium adjacent to left upper pulmonary veins (as indicated by the white arrow). LV, left ventricle.

Alarmingly, the patient discontinued all antihypertensive and anticoagulant medications post-discharge. He represented 10 months later with recurrent hypertensive emergency featuring prior symptoms plus new neurological deficits. Examination revealed extreme hypertension (210/140 mmHg). TTE showed progressive LA enlargement (LA anteroposterior diameter: 58 mm) with LV dilation (LVEDD: 54 mm) and reduced LVEF (42%) (Table 2). Critically, two new thrombi were identified: a 21 mm × 18 mm mass anchored at the middle-lower anterior wall of the LV (Figure 1C), and a separate 20 mm × 18 mm thrombus near the left upper pulmonary vein in the posterior LA (Figure 1D). Laboratory parameters are detailed in Table 1. Therapeutic reinitiation included nifedipine, arotinolol, aspirin, and low molecular weight heparin. Both thrombi diminished significantly by 2 weeks and resolved completely on 1-month TTE.

Throughout 6 years of subsequent follow-up with strict medication adherence, his BP stabilized around 160/95 mmHg. We observed gradual cardiac chamber size reduction without further thrombotic events, yet residual neurological impairment and renal dysfunction persisted. This case received approval from the Ethics Committee of the Affiliated Hospital of Shandong University of Traditional Chinese Medicine, with written informed consent provided by the patient.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was provided by the patient for the publication of this article and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

We document an exceptionally rare case of recurrent intracardiac thrombus formation in a young adult with poorly controlled hypertensive emergencies, representing the first known report of such repetitive thrombotic events despite transient resolution following anticoagulation. This distinctive clinical course highlights the crucial diagnostic value of serial TTE in both initial evaluation and long-term surveillance for hypertensive emergency patients developing cardiac thrombi.

Several interconnected mechanisms explain thrombogenesis here: first, the profound endothelial injury characteristic of hypertensive crises promotes fibrin deposition and platelet aggregation, establishing the pathological substrate for thrombus development (5). Second, sustained pressure overload induces significant LV hypertrophy and hyper-trabeculation, a finding objectively demonstrated in our patient where septal thickness reached 16 mm alongside prominent trabecular networks at the apex. These structural alterations create stagnant blood pools within deep intertrabecular recesses, directly enabling intraventricular thrombosis. Third, uncontrolled hypertension exceeding 160 mmHg precipitates heart failure (9), itself a recognized independent risk factor for intracardiac stasis and thrombus formation. The patient’s self-discontinuation of antihypertensive therapy critically underscores how therapeutic non-adherence heightens vulnerability to heart failure recurrence, confirming that sustained BP control constitutes an absolute therapeutic imperative.

TTE provides unparalleled clinical utility for such scenarios, delivering greater than 90% diagnostic accuracy in thrombus detection through its capacity to distinguish true thrombi (appearing as non-mobile masses separate from papillary muscles, chordae, or trabeculae) from technical artifacts (10). Its rapid bedside evaluation of structural and functional cardiac parameters makes it indispensable for guiding real-time management decisions. Consequently, we contend that TTE should constitute an indispensable component of the initial assessment for hypertensive emergencies, particularly given that this case establishes the previously undocumented risk of thrombus recurrence. Mandatory serial TTE follow-up thus becomes essential for monitoring thrombus resolution or recrudescence. Cardiac magnetic resonance (CMR) provides enhanced detection of LV thrombi through its high spatial resolution and tissue characterization capabilities, such as late gadolinium enhancement, which can differentiate thrombi from myocardial structures more reliably than echocardiography alone. Incorporating CMR in follow-up assessments could improve diagnostic confidence and inform anticoagulation strategies in high-risk patients with recurrent thrombotic events. In this case, TTE was selected over CMR because the thrombus was clearly identifiable on echocardiography, obviating the need for advanced imaging. Additionally, given the patient’s concurrent heart failure, TTE offered expedient assessment of cardiac function, aligning with urgent clinical priorities.

This case compellingly demonstrates that disciplined antihypertensive adherence is a key factor influencing prognosis in thrombus-prone hypertensive emergencies. The patient’s lapse in treatment directly triggered recurrent thromboembolism despite initial anticoagulation success, whereas consistent medication later prevented recurrence despite suboptimal BP control. These observations establish three cardinal principles: first, in the long-term management of such patients, sustained BP control is critical for preventing recurrent intracardiac thrombosis; second, serial TTE remains irreplaceable for detecting occult thrombus formation prior to irreversible complications; third, young patients warrant aggressive surveillance given their catastrophic thromboembolic risk from therapeutic negligence. This experience mandates integrating structured medication compliance programs with scheduled echocardiographic monitoring as a new clinical paradigm for this vulnerable population.

Acknowledgments

None.

Footnote

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://qims.amegroups.com/article/view/10.21037/qims-2025-1706/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this article and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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