Case

A 60 -year - old male patient was directly brought into our catherization laboratory on the suspicion of a heart attack with the chief complaints of increasing shortness of breath and a short - lasting chest pain. A 12 - lead surface ECG showed ST - segment elevations in aVR, V1 and V2, so a cardiogenic shock due to myocardial infarction (STEMI) was primarily assumed. At the same time laboratory and clinical findings indicated relevant abnormalities (Table 1) in light of a right heart failure verified by transthoracic echocardiography (Table 1, Figure 1A). Only a mild single vessel coronary artery disease (mid LAD) was revealed that required no intervention. The patient’s shock aggravated now with an elevated arterial lactate of 3.5 mmol / L, requiring an inotropic therapy (Table 1) and volume substitution (400 ml/h) to maintain a mean blood pressure of 60 – 70 mmHg. It was decided to perform an additional catheter based pulmonary angiography on account of highly likely hemodynamically relevant pulmonary embolism. A massive bilateral embolism was found cutting of most of the blood flow to the lung with a significantly raised pulmonary artery pressure (sPAP/dPAP/mPAP: 44 / 23 / 29 mmHg). A further decision was made favoring immediate interventional treatment using the FlowTriever device (INARI Medical) for direct thrombus aspiration. The left pulmonary artery was targeted first. Immediately after the fourth aspiration cycle the circulation shifted towards more and more hypertensive blood pressure values (systolic pressure > 150 mmHg) and the volume rate of the inotropic therapy and fluid substitution could be dramatically reduced. The patient was increasingly relived from shortness of breath. After 30 minutes, a total of 18 aspiration cycles removed most of the thrombotic material from both pulmonary arteries (Figure 1B). The retrieved material was partly fresh and partly already organized.  During the intervention an activated clotting time (ACT) of over 300s was maintained via intravenous unfractioned heparin. Already after the procedure and still inside the catheterization laboratory, all inotropes and volume resuscitation could be stopped. Arterial blood gas analysis showed a normalized lactate of 1.5 mmol/L. Vital signs improved as well (Table 1) and O₂ supplementation could be deescalated to a nasal cannula. PAK - hemodynamics confirmed the improved pulmonary circulation (Table 1). During the entire procedure the patient was adequately awake (GCS of 15). The patient was intermittently transferred in stable hemodynamic conditions (Table 1) to our intensive care unit (ICU) for postinterventional monitoring and continuation of intravenous unfractioned heparin application (target aPTT: 60 – 70s). A CT -angiography of the pulmonary circulation after the procedure verified only minor residual subsegmental thrombotic material. Until discharge, relevant clinical, ECG, echocardiography (Figure 1C) and laboratory parameters returned to or near normal ranges (Table 1) and a 6 - minute - walking test (6MWT) showed no pulmonary limitations or oxygenation impairments (distance: 420m; pO₂: 78.09 mmHg  = 10.54kPa)).

Conclusion

Direct percutaneous thrombectomy even during cardiogenic shock is feasible however depending on local expertise and resources. It could be demonstrated that such an approach leads to almost immediate reversal of all shock signs and symptoms and uncompromised recovery of the patient.