The clinical symptoms of PE are diverse and lack specificity, with studies showing that approximately 5–10% of patients mainly present with chest pain and dyspnea. In addition, PE patients can also present with shortness of breath, syncope, cyanosis, etc. While the so-called “triad of acute pulmonary embolism”, namely dyspnea, chest pain, and hemoptysis, are infrequently encountered3. Consequently, the non-specific clinical symptoms accompanied by ECG changes, often complicates the diagnosetic process, leading to misdiagnosis, particularly with CHD. In the presented case, the patient initially exhibited an episode of chest tightness, which was relieved after rest.
This is a typical manifestation of UA pectoris of CHD. After admission, a thorough examination showed that D-dimer was 0.90mg/L, which was elevated, and ECG showed right heart dysfunction, mild tricuspid regurgitation, moderate pulmonary hypertension and impaired left ventricular diastolic function, so PE was suspected and subsequently confirmed via CTPA, which revealed multiple pulmonary embolism in both lungs. Therefore, when patients present with chest pain or tightness after activity accompanied by abnormal ECG, in addition to considering CHD, angina pectoris and myocardial infarction, PE must also be considered as a differential diagnosis. Patients suspected of PE should first undergo arterial blood gas analysis to assess hypoxemia4.In addition, D-dimer should also be checked in time, which serve as pivotal diagnostic adjunct. The sensitivity of D-dimer to PE diagnosis is high, up to 92–100%, but the specificity is low, only 40–43%. Therefore, negative D-dimer can be used as an exclusion index for PE diagnosis. If D-dimer is less than 500µg/L, PE can be basically ruled out; If D-dimer is elevated, CTPA can be used to further confirmed the diagnosis5. Owing to its non-invasive nature, high sensitivity and specificity, CTPA has replaced conventional gold standard, that is pulmonary arteriography, and become the preferred diagnostic method6.
For both cardiovascular events and PE, high vascular inflammation and blood hypercoagulability are the basis of embolic events, while some common risk factors, such as smoking, obesity, hypertension and hyperlipidemia, can exacerbate vascular inflammation, at the same time disrupt the balance of procoagulant and anticoagulant factors in the bloodstream, increasing blood viscosity, thereby promoting the occurrence of embolic events7,8. Emboli that cause PE may originate from various anatomical sources including the inferior vena cava, superior vena cava, or right cardiac chamber, with a predominant origin from the deep veins of the lower extremities. Notably, in this case, colored doppler ultrasound of lower limb vein revealed no obvious abnormalities, while the colored doppler ultrasound of lower limb arteries indicated the presence of calcification spots without concurrent thrombosis. Moreover, this patient underwent CABG, employing LIMA and great saphenous vein as bridging vessels. For patients with CHD, although CABG is of great significance for the treatment and improvement of their quality of life, the surgery also causes inherent risks including vascular trauma and prolonged postoperative immobilization, which predispose patients venous thrombosis. Du et al. conducted a clinical study that included a total of 8956 patients undergoing CABG, among which the incidence of postoperative VTE was 1.75%, PE was 0.61%, DVT was 1.28%, and 0.15% of patients experienced both two conditions within 30 days after surgery9. Furthermore, post-CABG patients may experience dyspnea and pleural effusion due to sternal pain and pleural exudate, which may potentially mask the clinical manifestations of PE and lead to underdiagnosis of PE. Therefore, patients after CABG should take early exercise, mechanical prophylaxis such as graduated compression stockings (GCS), intermittent pneumatic compression (IPC) devices, or pharmacological prophylaxis such as subcutaneous heparin injection to prevent VTE10.
For individual cases of CHD combined with PE, clinical reports are not rare in recent years11,12. The diagnosis and treatment of patients with the combination of two diseases are often complicated, and the key to ensure accurate diagnosis is to improve the clinicians' understanding of the clinical manifestations and pathophysiology of PE, enhance the awareness of differential diagnosis of CHD and PE, pay attention to its risk factors, and rationally use laboratory or imaging examinations. If a patient is suspected of having PE, firstly, arterial blood phase analysis and D-dimer examination should be performed as soon as possible. Secondly, early echocardiography should be performed, which is an important tool for risk stratification and identification of other fatal diseases such as aortic dissection. For definitive diagnosis, radionuclide ventilation/perfusion scanning or CTPA should be performed. In addition, for patients manifesting typical symptoms of CHD, CAG is recommended as soon as possible to determine the following treatment plan.
Based on this case, we summarized the following experiences in the treatment of CHD combined with PE. Firstly, the treatment of patients with CHD complicated by PE should emphasize two aspects at the same time. On the one hand, anticoagulant therapy such as low molecular weight heparin or warfarin should be given, on the other hand, antiplatelet therapy such as aspirin or clopidogrel should also be given. Anticoagulant drugs have been shown to reduce the risk of thrombotic events in the arteries, and antiplatelet drugs and low-dose anticoagulants have also been recommended by the European Heart Association for secondary prevention in indibiduals with chronic coronary syndrome13. Secondly, we should take individualized treatment strategy after comprehensively assessing patient's overall condition. If PE presents acutely, thrombolysis or anticoagulation therapy should be taken first, conversely, if CHD is more severe, percutaneous coronary intervention (PCI) or CABG should be performed first. In addition, we should follow up on time and pay close attention to the changes of the patient's condition in order to improve the patient's prognosis.