ArticleCureus2025
Pulmonary Embolism in a Patient With Undifferentiated Dyspnoea.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Pulmonary embolism can cause right and left ventricular dysfunction and induce acute heart failure or shock. A 76-year-old gentleman with a history of ischaemic heart disease and atrial fibrillation, on oral warfarin and clopidogrel daily, presented with a three-day history of worsening shortness of breath associated with a dull ache over the right side of his chest. On examination, auscultation of his lungs revealed mild crepitations bilaterally at the bases and bilateral pitting oedema of legs up to his shins. His ECG showed ST-segment depression in lead 1, aVL, V2 to V6. His Chest X-ray showed cardiomegaly with minimal bilateral lower zone haziness. The initial provisional diagnosis was decompensated heart failure, and the patient was referred to acute medicine. His blood tests later showed a white cell count (WCC) of 15, CRP 298 and D-Dimer of 35317. This was followed by a computed tomography (CT) pulmonary angiogram, which showed multiple bilateral proximal pulmonary emboli with right heart strain. A massive pulmonary embolism can present with non-specific signs and symptoms, which makes it difficult to diagnose. Clinicians should maintain a high index of suspicion as a patient on blood thinner cannot be excluded from having a pulmonary embolism. Acute heart failure and pulmonary embolism can clinically present in a similar way and often share similar risk factors. The patient developed a pulmonary embolism despite being on both warfarin (anticoagulation) and clopidogrel (antiplatelet). Even with the latest advanced therapies and anticoagulation therapies, mortality remains high. Patients who have received a direct-acting oral anticoagulant (DOAC) will have significantly lower rates of progression to a pulmonary embolism than those on warfarin. Many factors can affect the therapeutic effect of warfarin. This case showed that pulmonary embolism can occur despite dual anticoagulant and antiplatelet therapy, particularly when therapy is subtherapeutic. It also highlights the importance of maintaining high clinical suspicion for pulmonary embolism even in patients who are taking anticoagulation therapy or dual anticoagulation and antiplatelet therapy. It suggests that DOACs may provide more reliable anticoagulation than warfarin in selected patients.
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