A Non-Stenting Approach to Left Main Thrombus in an Oncology Patient with Acute Heart Failure: A Case Report

Introduction

Cancer patients face a heightened risk of cardiovascular disease, particularly acute coronary syndrome (ACS). The co-existence of cancer and cardiovascular risk factors creates a complex clinical picture, impacting treatment strategies and leading to increased mortality. Among cancer survivors, cardiovascular disease is a leading cause of late complications. This overlap can result from the chronic inflammation associated with malignancies and the cardiotoxic effects of cancer therapies, which can accelerate atherosclerosis and lead to endothelial dysfunction, coronary thrombosis, and vasospasm [1]

The dual presence of ACS and cancer significantly worsens prognosis, making treatment especially challenging and management should be individualized. Decisions must consider not only the ACS subtype but also the cancer type and stage, bleeding and thrombotic risks, life expectancy, ongoing or planned cancer treatments, and overall clinical stability [2]. If life expectancy exceeds 6 months and instability is present, early PCI is advised. A conservative approach may be suitable for stable N-STEMI patients with poor prognosis or high bleeding risk due to metastases, thrombocytopenia, or coagulopathies [1,2].

Managing acute heart failure resulting from myocardial infarct in oncology patients can be challenging, as numerous clinical and therapeutic decisions must be made. We present a rare case of a 70-year-old man with a history of prostate cancer who developed cardiogenic shock due to N-STEMI with significant thrombotic burden in the LM bifurcation.

Case Report

HISTORY OF PRESENTATION:

A 70-year-old man was admitted to the Coronary Care Unit (CCU) with chest pain, dyspnea, and hypotension. He had been hospitalized for the last 6 days in the Urology Department with fever and a urinary tract infection. He underwent prostatectomy 7 months ago and had received radiotherapy for cancer. Since then, he had been hospitalized several times for a recurrent urinary tract infection. During his most recent admission, a lung metastasis secondary to prostate cancer was identified.

On admission, his blood pressure was 75/50mmHg and his heart rate was 120 beats per min (regular rhythm). His body temperature was 36.6 Co. Physical examination revealed cold extremities, lower-limb swelling, and a dilated jugular vein. Bilateral basal crackles were heard. He also had oliguria.

The 12-lead electrocardiogram (ECG) demonstrated sinus tachycardia with first-degree heart block, poor R wave progression in V1–V6 leads, and negative T waves in leads I, AVL,V4, V5, and V6 (new changes). A chest X-ray showed an enlarged cardiac silhouette, an increased cardiothoracic ratio, and upper-lobe pulmonary venous diversion. Arterial blood gas analysis showed saturation at 91% on ambient air and blood lactate concentration 3.6 mmol/L.

PAST MEDICAL HISTORY:

He had a history of arterial hypertension, dyslipidemia, and type II diabetes mellitus. Eight years ago, he underwent a PCI with a DES in the LAD due to stable angina. Six years ago, he underwent aortic valve replacement with a bioprosthetic valve due to severe aortic stenosis.

DIFFERENTIAL DIAGNOSIS:

The initial differential diagnosis included acute coronary syndrome without ST elevation, acute aortic syndrome, and pulmonary embolism. Pulmonary embolism had been excluded in the Urology Department by performing a computed tomography (CT) pulmonary angiography.

INVESTIGATIONS:

Echocardiogram revealed severe left ventricular (LV) systolic dysfunction (ejection fraction: 30%) with normal LV diameters, akinesia of anterior, basal, and mid-anterolateral wall and apex, with high filling pressure of LV, moderate-to-severe mitral (MR) and tricuspid regurgitation (TR), borderline RV function (TAPSE: 16 mm), and no pericardial fluid.

His laboratories test results at admission were: hemoglobin (Hb): 8.6%, white blood cells (WBC): 6,460×10³/μl, platelets (PLT): 127000, creatinine (CR): 2.20 mg/dl (eGFR: 31 ml/min/1.73 m²), urea (Ur): 65 mg/dl, sodium (NA): 130 mEq/L, potassium (K): 5,3 mEq/L, lactate dehydrogenase (LDH): 403 U/L, international normalized ratio (INR): 1.15, high-sensitivity cardiac troponin I 46 527.9 pg/mL, and C-reactive protein 25 mg/L.

MANAGEMENT:

The patient was diagnosed with cardiogenic shock due to N-STEMI. He was clinically unstable, presenting with persistent chest discomfort, low blood pressure, narrow pulse pressure, low urine output, and elevated lactates in arterial blood gas analysis. He was therefore transferred to the catheterization lab.

Coronary angiography via the right femoral artery revealed a severe thrombotic lesion with a significant thrombus burden in the LM causing subtotal stenosis at the ostia of the LAD and LCX arteries (Figure 1, Video 1). A loading dose of clopidogrel (600 mg) was administered (he was already on aspirin) and an intraortic balloon pump (IABP) (Impella was not available) was implanted via the left femoral artery, as intravenous vasoconstrictors (norepinephrine) and inotropes (dobutamine) were already started but the blood pressure remained low. A 7Fr XB 4.0 guide catheter was used to catheterize the left coronary artery and Tirofiban was administered (a bolus of 33 mg intra-coronary followed by intravenous infusion with 12 ml/h). Within 5 minutes of the bolus infusion, there was a significant improvement in coronary flow in both arteries (Figure 2). Next, we pre-dilated the LAD-LCX with a semi-compliant 2.5×20 mm balloon and pre-dilated the LAD with a 3.0×15 mm semi-compliant balloon. Due to disturbance of oblique marginal (OM1) flow, we used a 2.0×20 mm semi-compliant balloon to dilate the OM1. Given the angiographic result with TIMI III flow and no angiographically severe atherosclerotic plaque causing residual stenosis, we decided to stop the procedure and not proceed to LM bifurcation stenting (Figure 2, Video 2).

OUTCOME AND FOLLOW-UP:

The patient was transferred to the CCU. Tirofiban was continued for the next 24 hours. The following day, ECG revealed a left bundle branch block (LBBB). On the third day, transthoracic echocardiography showed severe systolic dysfunction of the LV with akinesia of all LV walls except the basal and mid-anterolateral and basal anterior wall (LV ejection fraction: 20%), borderline filling pressure of the LV, moderate MR and TR, borderline function of the right ventricle (TAPSE: 17 mm), pulmonary artery systolic pressure 40–45 mmHg, and no pericardial fluid. However, the patient was stable and the IABP was removed. On the fourth day, an ECG revealed complete heart block. An emergency permanent pacemaker generator with defibrillation capable leads were placed, as the patient might meet the criteria for an ICD in the near future, but without the ICD generator as there had been no ventricular tachycardia up to this time, and he did not receive optimal medical therapy for at least 6 weeks.

Over the following days, he had gradual clinical improvement. He remained hemodynamically stable with satisfactory diuresis and no arrhythmias noted on continuous monitoring. Serial echocardiograms showed an improvement of LV function (LV ejection fraction 35%, normal filling pressure of the LV, mild MR-TR, TAPSE 17 mm). Six days after the event, a new coronary angiography was performed, this time with intravascular imaging, which had not been performed initially due to the presence of a significant thrombotic burden. The objective was to re-evaluate the left coronary artery and assess for the presence of any significant dissections or stenoses that might necessitate further intervention with stent implantation. No angiographically significant stenosis was identified in the LM and at the ostia of the LAD and LCX. A 50% stenosis that was revealed distal of the previous stent in LAD and LCX was occluded distally. Intravascular ultrasound (IVUS, Boston Scientific-OpticCross HD) showed the minimal lumen area (MLA) for LM was 13.92 mm2, 8.81 mm2 for LAD, and 11.8 mm2 for LCX, without dissections (Figure 3, Videos 3, 4).

The patient was discharged in clinically stable condition. He was advised to be treated with dual antiplatelet therapy (DAPT) for at least 1 year, statin with LDL target <55 mg/dl, beta-blocker (metoprolol 100 mg ¼ twice daily), eplerenone 25 mg once daily, and furosemide 40 mg once daily. He was advised to have close follow-up in the heart failure clinic. SGLT-2 inhibitors were not started due to the recent history urinary tract infection. Furthermore, ACE inhibitor could not be tolerated due to low blood pressure.

At 3-month follow-up, he was clinically stable with NYHA Class II–III and echocardiography did not show further significant improvement of the left ventricle systolic function. Finally, 7 months after the event, he required hospitalization for 6 weeks due to infective endocarditis (Enterococcus faecalis) of the bioprosthetic aortic valve. In addition, he underwent splenectomy due to splenic abscess caused by septic emboli. Aspirin was continued perioperatively and indefinitely.

Discussion

The combination of acute heart failure and cardiogenic shock due to acute myocardial infarction is usually fatal if not treated immediately. Oncology patients may have a large thrombotic burden in the culprit lesion, and plain balloon angioplasty could be a reasonable alternative to stenting in these patients, especially when there is no severe coronary stenosis [3,4]. Moreover, the risk of coronary stent thrombosis is higher in cancer patients [5].

Use of a drug-coated balloon could be another option, although there is no evidence of better outcomes compared to plain balloons in patients with thrombotic but no stenotic lesions [6,7].

Randomized controlled trials have shown that intravascular imaging-guided PCI compared with angiography-guided PCI is associated with better clinical outcomes in non-complex and complex coronary lesions [8], but cancer patients were excluded from these studies. However, according to 2023 ESC guidelines for the management of acute coronary syndromes, an invasive strategy is recommended in cancers patients with acute coronary syndrome who have life expectancy ≥6 months, or irrespective of the prognosis if the patient is unstable. Taking this into consideration, we proceeded to treat the patient with the same approach and standards applied to individuals without cancer, ensuring consistency in care despite the lack of cancer-specific data. Moreover, intra-coronary imaging with optical coherence tomography revealed that plaque erosion is the most frequent underlying mechanism of an acute coronary syndrome in patients with cancer, and this might influence the decision to use PCI in ACS patients [9,10]. Because our patient had stage 4 chronic kidney disease (eGFR 25 ml/min), we did not perform optical coherence tomography, since the plaque erosion was not revealed in our IVUS study, but conventional IVUS cannot easily identify it. OCT provides superior resolution compared to conventional IVUS, allowing for detailed visualization of superficial plaque characteristics such as fibrous cap integrity and thrombus presence, which are crucial in diagnosing plaque erosion. IVUS, while useful for assessing plaque burden and vessel dimensions, lacks the resolution to detect subtle surface changes, limiting its diagnostic utility in erosion. In our patient, despite the absence of OCT, IVUS offered compensatory value by delineating plaque morphology and exclusion of residual severe disease or dissection and guiding therapeutic decisions.

The use of intra-coronary and intravenous antiplatelet drugs in patients with acute coronary syndrome and thrombotic lesions can be a valuable and often necessary adjunctive therapeutic strategy. In our case, as we had to deal with a heavy thrombotic burden, we decided it would benefit our patient to administer oral clopidogrel and intra-coronary Tirofiban as IIb/IIIa agent (bailout angioplasty) to have different paths of platelets inhibition. To avoid thrombus embolization downstream, thrombectomy aspiration was not performed. In addition, the TOTAL optical coherence tomography substudy showed no differences in residual thrombus volume in patients treated with thrombectomy vs balloon angioplasty [11].

Our patient had a high bleeding risk according to the ARC-HBR criteria (active cancer, eGFR 31 ml/min/1.73 m2, Hb 8.6%); therefore, DAPT with aspirin and clopidogrel was selected instead of newer P2Y12 antagonists. However, data are lacking and real-world data suggest that potent P2Y12i can have a similar bleeding risk compared to clopidogrel in cancer patients undergoing PCI [12]. Considering that IVUS did not reveal any significant stenosis or dissection, and considering the increased risk of unplanned future surgery in cancer patients, stent implantation was deferred to preserve the option of discontinuing dual antiplatelet therapy if clinically required [1]. Indeed, due to a non-cardiac surgery, DAPT was stopped after 7 months, followed by life-long aspirin monotherapy. Regarding our strategy, the DANAMI-3 DEFER study showed that in STEMI patients who achieved TIMI III flow following initial balloon angioplasty, and who showed no significant residual stenosis, thrombus, or dissection at re-evaluation 48 hours later, outcomes were comparable whether or not a stent was implanted. This was confirmed over a median follow-up period of 3.4 years, with no significant difference in adverse events between the 2 groups [4]. However, data on this strategy in cancer patients are lacking.

Conclusions

Interventional cardiologists have many tools for treatment of coronary artery disease and cardiogenic shock. However, the key lies in tailoring their use to the individual patient’s clinical status and life expectancy, particularly in oncology patients, for whom therapeutic decisions must be guided by performance status and overall prognosis. Cancer is not a contraindication for invasive treatment of patients presenting with acute coronary syndrome. Plain balloon angioplasty can be considered in patients with a large thrombotic burden, no residual stenosis, and no plaque erosion or dissection confirmed by intravascular imaging. Intravascular imaging is crucial before a definite decision is made.